Interplay Between Primary Cilia and Autophagy and Its Controversial Roles in Cancer
Identifieur interne : 000872 ( Pmc/Corpus ); précédent : 000871; suivant : 000873Interplay Between Primary Cilia and Autophagy and Its Controversial Roles in Cancer
Auteurs : Je Yeong Ko ; Eun Ji Lee ; Jong Hoon ParkSource :
- Biomolecules & Therapeutics [ 1976-9148 ] ; 2019.
Abstract
Primary cilia and autophagy are two distinct nutrient-sensing machineries required for maintaining intracellular energy homeostasis, either via signal transduction or recycling of macromolecules from cargo breakdown, respectively. Potential correlations between primary cilia and autophagy have been recently suggested and their relationship may increase our understanding of the pathogenesis of human diseases, including ciliopathies and cancer. In this review, we cover the current issues concerning the bidirectional interaction between primary cilia and autophagy and discuss its role in cancer with cilia defect.
Url:
DOI: 10.4062/biomolther.2019.056
PubMed: 31042678
PubMed Central: 6609109
Links to Exploration step
PMC:6609109Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Interplay Between Primary Cilia and Autophagy and Its Controversial Roles in Cancer</title><author><name sortKey="Ko, Je Yeong" sort="Ko, Je Yeong" uniqKey="Ko J" first="Je Yeong" last="Ko">Je Yeong Ko</name></author><author><name sortKey="Lee, Eun Ji" sort="Lee, Eun Ji" uniqKey="Lee E" first="Eun Ji" last="Lee">Eun Ji Lee</name></author><author><name sortKey="Park, Jong Hoon" sort="Park, Jong Hoon" uniqKey="Park J" first="Jong Hoon" last="Park">Jong Hoon Park</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31042678</idno><idno type="pmc">6609109</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6609109</idno><idno type="RBID">PMC:6609109</idno><idno type="doi">10.4062/biomolther.2019.056</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000872</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000872</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Interplay Between Primary Cilia and Autophagy and Its Controversial Roles in Cancer</title><author><name sortKey="Ko, Je Yeong" sort="Ko, Je Yeong" uniqKey="Ko J" first="Je Yeong" last="Ko">Je Yeong Ko</name></author><author><name sortKey="Lee, Eun Ji" sort="Lee, Eun Ji" uniqKey="Lee E" first="Eun Ji" last="Lee">Eun Ji Lee</name></author><author><name sortKey="Park, Jong Hoon" sort="Park, Jong Hoon" uniqKey="Park J" first="Jong Hoon" last="Park">Jong Hoon Park</name></author></analytic><series><title level="j">Biomolecules & Therapeutics</title><idno type="ISSN">1976-9148</idno><idno type="eISSN">2005-4483</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Primary cilia and autophagy are two distinct nutrient-sensing machineries required for maintaining intracellular energy homeostasis, either via signal transduction or recycling of macromolecules from cargo breakdown, respectively. Potential correlations between primary cilia and autophagy have been recently suggested and their relationship may increase our understanding of the pathogenesis of human diseases, including ciliopathies and cancer. In this review, we cover the current issues concerning the bidirectional interaction between primary cilia and autophagy and discuss its role in cancer with cilia defect.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Agbu, So" uniqKey="Agbu S">SO Agbu</name></author><author><name sortKey="Liang, Y" uniqKey="Liang Y">Y Liang</name></author><author><name sortKey="Liu, A" uniqKey="Liu A">A Liu</name></author><author><name sortKey="Anderson, Kv" uniqKey="Anderson K">KV Anderson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Alers, S" uniqKey="Alers S">S Alers</name></author><author><name sortKey="Loffler, As" uniqKey="Loffler A">AS Loffler</name></author><author><name sortKey="Wesselborg, S" uniqKey="Wesselborg S">S Wesselborg</name></author><author><name sortKey="Stork, B" uniqKey="Stork B">B Stork</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Avalos, Y" uniqKey="Avalos Y">Y Avalos</name></author><author><name sortKey="Pena Oyarzun, D" uniqKey="Pena Oyarzun D">D Pena-Oyarzun</name></author><author><name sortKey="Budini, M" uniqKey="Budini M">M Budini</name></author><author><name sortKey="Morselli, E" uniqKey="Morselli E">E Morselli</name></author><author><name sortKey="Criollo, A" uniqKey="Criollo A">A Criollo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Basten, Sg" uniqKey="Basten S">SG Basten</name></author><author><name sortKey="Giles, Rh" uniqKey="Giles R">RH Giles</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Basten, Sg" uniqKey="Basten S">SG Basten</name></author><author><name sortKey="Willekers, S" uniqKey="Willekers S">S Willekers</name></author><author><name sortKey="Vermaat, Js" uniqKey="Vermaat J">JS Vermaat</name></author><author><name sortKey="Slaats, Gg" uniqKey="Slaats G">GG Slaats</name></author><author><name sortKey="Voest, Ee" uniqKey="Voest E">EE Voest</name></author><author><name sortKey="Van Diest, Pj" uniqKey="Van Diest P">PJ van Diest</name></author><author><name sortKey="Giles, Rh" uniqKey="Giles R">RH Giles</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Battle, C" uniqKey="Battle C">C Battle</name></author><author><name sortKey="Ott, Cm" uniqKey="Ott C">CM Ott</name></author><author><name sortKey="Burnette, Dt" uniqKey="Burnette D">DT Burnette</name></author><author><name sortKey="Lippincott Schwartz, J" uniqKey="Lippincott Schwartz J">J Lippincott-Schwartz</name></author><author><name sortKey="Schmidt, Cf" uniqKey="Schmidt C">CF Schmidt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cao, M" uniqKey="Cao M">M Cao</name></author><author><name sortKey="Zhong, Q" uniqKey="Zhong Q">Q Zhong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Chaya, T" uniqKey="Chaya T">T Chaya</name></author><author><name sortKey="Omori, Y" uniqKey="Omori Y">Y Omori</name></author><author><name sortKey="Kuwahara, R" uniqKey="Kuwahara R">R Kuwahara</name></author><author><name sortKey="Furukawa, T" uniqKey="Furukawa T">T Furukawa</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cloonan, Sm" uniqKey="Cloonan S">SM Cloonan</name></author><author><name sortKey="Lam, Hc" uniqKey="Lam H">HC Lam</name></author><author><name sortKey="Ryter, Sw" uniqKey="Ryter S">SW Ryter</name></author><author><name sortKey="Choi, Am" uniqKey="Choi A">AM Choi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Dasgupta, A" uniqKey="Dasgupta A">A Dasgupta</name></author><author><name sortKey="Amack, Jd" uniqKey="Amack J">JD Amack</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Delaine Smith, Rm" uniqKey="Delaine Smith R">RM Delaine-Smith</name></author><author><name sortKey="Sittichokechaiwut, A" uniqKey="Sittichokechaiwut A">A Sittichokechaiwut</name></author><author><name sortKey="Reilly, Gc" uniqKey="Reilly G">GC Reilly</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Glick, D" uniqKey="Glick D">D Glick</name></author><author><name sortKey="Barth, S" uniqKey="Barth S">S Barth</name></author><author><name sortKey="Macleod, Kf" uniqKey="Macleod K">KF Macleod</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Higgins, M" uniqKey="Higgins M">M Higgins</name></author><author><name sortKey="Obaidi, I" uniqKey="Obaidi I">I Obaidi</name></author><author><name sortKey="Mcmorrow, T" uniqKey="Mcmorrow T">T McMorrow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Hsiao, Cj" uniqKey="Hsiao C">CJ Hsiao</name></author><author><name sortKey="Chang, Ch" uniqKey="Chang C">CH Chang</name></author><author><name sortKey="Ibrahim, Rb" uniqKey="Ibrahim R">RB Ibrahim</name></author><author><name sortKey="Lin, Ih" uniqKey="Lin I">IH Lin</name></author><author><name sortKey="Wang, Ch" uniqKey="Wang C">CH Wang</name></author><author><name sortKey="Wang, Wj" uniqKey="Wang W">WJ Wang</name></author><author><name sortKey="Tsai, Jw" uniqKey="Tsai J">JW Tsai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jenks, Ad" uniqKey="Jenks A">AD Jenks</name></author><author><name sortKey="Vyse, S" uniqKey="Vyse S">S Vyse</name></author><author><name sortKey="Wong, Jp" uniqKey="Wong J">JP Wong</name></author><author><name sortKey="Kostaras, E" uniqKey="Kostaras E">E Kostaras</name></author><author><name sortKey="Keller, D" uniqKey="Keller D">D Keller</name></author><author><name sortKey="Burgoyne, T" uniqKey="Burgoyne T">T Burgoyne</name></author><author><name sortKey="Shoemark, A" uniqKey="Shoemark A">A Shoemark</name></author><author><name sortKey="Tsalikis, A" uniqKey="Tsalikis A">A Tsalikis</name></author><author><name sortKey="De La Roche, M" uniqKey="De La Roche M">M de la Roche</name></author><author><name sortKey="Michaelis, M" uniqKey="Michaelis M">M Michaelis</name></author><author><name sortKey="Cinatl, J" uniqKey="Cinatl J">J Cinatl</name></author><author><name sortKey="Huang, Ph" uniqKey="Huang P">PH Huang</name></author><author><name sortKey="Tanos, Be" uniqKey="Tanos B">BE Tanos</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jonassen, Ja" uniqKey="Jonassen J">JA Jonassen</name></author><author><name sortKey="San Agustin, J" uniqKey="San Agustin J">J San Agustin</name></author><author><name sortKey="Follit, Ja" uniqKey="Follit J">JA Follit</name></author><author><name sortKey="Pazour, Gj" uniqKey="Pazour G">GJ Pazour</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Jonassen, Ja" uniqKey="Jonassen J">JA Jonassen</name></author><author><name sortKey="Sanagustin, J" uniqKey="Sanagustin J">J SanAgustin</name></author><author><name sortKey="Baker, Sp" uniqKey="Baker S">SP Baker</name></author><author><name sortKey="Pazour, Gj" uniqKey="Pazour G">GJ Pazour</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kasahara, K" uniqKey="Kasahara K">K Kasahara</name></author><author><name sortKey="Kawakami, Y" uniqKey="Kawakami Y">Y Kawakami</name></author><author><name sortKey="Kiyono, T" uniqKey="Kiyono T">T Kiyono</name></author><author><name sortKey="Yonemura, S" uniqKey="Yonemura S">S Yonemura</name></author><author><name sortKey="Kawamura, Y" uniqKey="Kawamura Y">Y Kawamura</name></author><author><name sortKey="Era, S" uniqKey="Era S">S Era</name></author><author><name sortKey="Matsuzaki, F" uniqKey="Matsuzaki F">F Matsuzaki</name></author><author><name sortKey="Goshima, N" uniqKey="Goshima N">N Goshima</name></author><author><name sortKey="Inagaki, M" uniqKey="Inagaki M">M Inagaki</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kihara, A" uniqKey="Kihara A">A Kihara</name></author><author><name sortKey="Kabeya, Y" uniqKey="Kabeya Y">Y Kabeya</name></author><author><name sortKey="Ohsumi, Y" uniqKey="Ohsumi Y">Y Ohsumi</name></author><author><name sortKey="Yoshimori, T" uniqKey="Yoshimori T">T Yoshimori</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, Es" uniqKey="Kim E">ES Kim</name></author><author><name sortKey="Shin, Jh" uniqKey="Shin J">JH Shin</name></author><author><name sortKey="Park, Sj" uniqKey="Park S">SJ Park</name></author><author><name sortKey="Jo, Yk" uniqKey="Jo Y">YK Jo</name></author><author><name sortKey="Kim, Js" uniqKey="Kim J">JS Kim</name></author><author><name sortKey="Kang, Ih" uniqKey="Kang I">IH Kang</name></author><author><name sortKey="Nam, Jb" uniqKey="Nam J">JB Nam</name></author><author><name sortKey="Chung, Dy" uniqKey="Chung D">DY Chung</name></author><author><name sortKey="Cho, Y" uniqKey="Cho Y">Y Cho</name></author><author><name sortKey="Lee, Eh" uniqKey="Lee E">EH Lee</name></author><author><name sortKey="Chang, Jw" uniqKey="Chang J">JW Chang</name></author><author><name sortKey="Cho, Dh" uniqKey="Cho D">DH Cho</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kim, J" uniqKey="Kim J">J Kim</name></author><author><name sortKey="Jo, H" uniqKey="Jo H">H Jo</name></author><author><name sortKey="Hong, H" uniqKey="Hong H">H Hong</name></author><author><name sortKey="Kim, Mh" uniqKey="Kim M">MH Kim</name></author><author><name sortKey="Kim, Jm" uniqKey="Kim J">JM Kim</name></author><author><name sortKey="Lee, Jk" uniqKey="Lee J">JK Lee</name></author><author><name sortKey="Heo, Wd" uniqKey="Heo W">WD Heo</name></author><author><name sortKey="Kim, J" uniqKey="Kim J">J Kim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Kobayashi, T" uniqKey="Kobayashi T">T Kobayashi</name></author><author><name sortKey="Itoh, H" uniqKey="Itoh H">H Itoh</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lechtreck, Kf" uniqKey="Lechtreck K">KF Lechtreck</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Lee, J" uniqKey="Lee J">J Lee</name></author><author><name sortKey="Yi, S" uniqKey="Yi S">S Yi</name></author><author><name sortKey="Kang, Ye" uniqKey="Kang Y">YE Kang</name></author><author><name sortKey="Chang, Jy" uniqKey="Chang J">JY Chang</name></author><author><name sortKey="Kim, Jt" uniqKey="Kim J">JT Kim</name></author><author><name sortKey="Sul, Hj" uniqKey="Sul H">HJ Sul</name></author><author><name sortKey="Kim, Jo" uniqKey="Kim J">JO Kim</name></author><author><name sortKey="Kim, Jm" uniqKey="Kim J">JM Kim</name></author><author><name sortKey="Kim, J" uniqKey="Kim J">J Kim</name></author><author><name sortKey="Porcelli, Am" uniqKey="Porcelli A">AM Porcelli</name></author><author><name sortKey="Kim, Ks" uniqKey="Kim K">KS Kim</name></author><author><name sortKey="Shong, M" uniqKey="Shong M">M Shong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, Zq" uniqKey="Liu Z">ZQ Liu</name></author><author><name sortKey="Lee, Jn" uniqKey="Lee J">JN Lee</name></author><author><name sortKey="Son, M" uniqKey="Son M">M Son</name></author><author><name sortKey="Lim, Jy" uniqKey="Lim J">JY Lim</name></author><author><name sortKey="Dutta, Rk" uniqKey="Dutta R">RK Dutta</name></author><author><name sortKey="Maharjan, Y" uniqKey="Maharjan Y">Y Maharjan</name></author><author><name sortKey="Kwak, S" uniqKey="Kwak S">S Kwak</name></author><author><name sortKey="Oh, Gt" uniqKey="Oh G">GT Oh</name></author><author><name sortKey="Byun, K" uniqKey="Byun K">K Byun</name></author><author><name sortKey="Choe, Sk" uniqKey="Choe S">SK Choe</name></author><author><name sortKey="Park, R" uniqKey="Park R">R Park</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Malicki, Jj" uniqKey="Malicki J">JJ Malicki</name></author><author><name sortKey="Johnson, Ca" uniqKey="Johnson C">CA Johnson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mauthe, M" uniqKey="Mauthe M">M Mauthe</name></author><author><name sortKey="Orhon, I" uniqKey="Orhon I">I Orhon</name></author><author><name sortKey="Rocchi, C" uniqKey="Rocchi C">C Rocchi</name></author><author><name sortKey="Zhou, X" uniqKey="Zhou X">X Zhou</name></author><author><name sortKey="Luhr, M" uniqKey="Luhr M">M Luhr</name></author><author><name sortKey="Hijlkema, Kj" uniqKey="Hijlkema K">KJ Hijlkema</name></author><author><name sortKey="Coppes, Rp" uniqKey="Coppes R">RP Coppes</name></author><author><name sortKey="Engedal, N" uniqKey="Engedal N">N Engedal</name></author><author><name sortKey="Mari, M" uniqKey="Mari M">M Mari</name></author><author><name sortKey="Reggiori, F" uniqKey="Reggiori F">F Reggiori</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Menzl, I" uniqKey="Menzl I">I Menzl</name></author><author><name sortKey="Lebeau, L" uniqKey="Lebeau L">L Lebeau</name></author><author><name sortKey="Pandey, R" uniqKey="Pandey R">R Pandey</name></author><author><name sortKey="Hassounah, Nb" uniqKey="Hassounah N">NB Hassounah</name></author><author><name sortKey="Li, Fw" uniqKey="Li F">FW Li</name></author><author><name sortKey="Nagle, R" uniqKey="Nagle R">R Nagle</name></author><author><name sortKey="Weihs, K" uniqKey="Weihs K">K Weihs</name></author><author><name sortKey="Mcdermott, Km" uniqKey="Mcdermott K">KM McDermott</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Mizushima, N" uniqKey="Mizushima N">N Mizushima</name></author><author><name sortKey="Yoshimori, T" uniqKey="Yoshimori T">T Yoshimori</name></author><author><name sortKey="Ohsumi, Y" uniqKey="Ohsumi Y">Y Ohsumi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Moon, H" uniqKey="Moon H">H Moon</name></author><author><name sortKey="Song, J" uniqKey="Song J">J Song</name></author><author><name sortKey="Shin, Jo" uniqKey="Shin J">JO Shin</name></author><author><name sortKey="Lee, H" uniqKey="Lee H">H Lee</name></author><author><name sortKey="Kim, Hk" uniqKey="Kim H">HK Kim</name></author><author><name sortKey="Eggenschwiller, Jt" uniqKey="Eggenschwiller J">JT Eggenschwiller</name></author><author><name sortKey="Bok, J" uniqKey="Bok J">J Bok</name></author><author><name sortKey="Ko, Hw" uniqKey="Ko H">HW Ko</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Nakatogawa, H" uniqKey="Nakatogawa H">H Nakatogawa</name></author><author><name sortKey="Ichimura, Y" uniqKey="Ichimura Y">Y Ichimura</name></author><author><name sortKey="Ohsumi, Y" uniqKey="Ohsumi Y">Y Ohsumi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Nobutani, K" uniqKey="Nobutani K">K Nobutani</name></author><author><name sortKey="Shimono, Y" uniqKey="Shimono Y">Y Shimono</name></author><author><name sortKey="Yoshida, M" uniqKey="Yoshida M">M Yoshida</name></author><author><name sortKey="Mizutani, K" uniqKey="Mizutani K">K Mizutani</name></author><author><name sortKey="Minami, A" uniqKey="Minami A">A Minami</name></author><author><name sortKey="Kono, S" uniqKey="Kono S">S Kono</name></author><author><name sortKey="Mukohara, T" uniqKey="Mukohara T">T Mukohara</name></author><author><name sortKey="Yamasaki, T" uniqKey="Yamasaki T">T Yamasaki</name></author><author><name sortKey="Itoh, T" uniqKey="Itoh T">T Itoh</name></author><author><name sortKey="Takao, S" uniqKey="Takao S">S Takao</name></author><author><name sortKey="Minami, H" uniqKey="Minami H">H Minami</name></author><author><name sortKey="Azuma, T" uniqKey="Azuma T">T Azuma</name></author><author><name sortKey="Takai, Y" uniqKey="Takai Y">Y Takai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Okada, Y" uniqKey="Okada Y">Y Okada</name></author><author><name sortKey="Nonaka, S" uniqKey="Nonaka S">S Nonaka</name></author><author><name sortKey="Tanaka, Y" uniqKey="Tanaka Y">Y Tanaka</name></author><author><name sortKey="Saijoh, Y" uniqKey="Saijoh Y">Y Saijoh</name></author><author><name sortKey="Hamada, H" uniqKey="Hamada H">H Hamada</name></author><author><name sortKey="Hirokawa, N" uniqKey="Hirokawa N">N Hirokawa</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pampliega, O" uniqKey="Pampliega O">O Pampliega</name></author><author><name sortKey="Cuervo, Am" uniqKey="Cuervo A">AM Cuervo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pampliega, O" uniqKey="Pampliega O">O Pampliega</name></author><author><name sortKey="Orhon, I" uniqKey="Orhon I">I Orhon</name></author><author><name sortKey="Patel, B" uniqKey="Patel B">B Patel</name></author><author><name sortKey="Sridhar, S" uniqKey="Sridhar S">S Sridhar</name></author><author><name sortKey="Diaz Carretero, A" uniqKey="Diaz Carretero A">A Diaz-Carretero</name></author><author><name sortKey="Beau, I" uniqKey="Beau I">I Beau</name></author><author><name sortKey="Codogno, P" uniqKey="Codogno P">P Codogno</name></author><author><name sortKey="Satir, Bh" uniqKey="Satir B">BH Satir</name></author><author><name sortKey="Satir, P" uniqKey="Satir P">P Satir</name></author><author><name sortKey="Cuervo, Am" uniqKey="Cuervo A">AM Cuervo</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Plotnikova, Ov" uniqKey="Plotnikova O">OV Plotnikova</name></author><author><name sortKey="Nikonova, As" uniqKey="Nikonova A">AS Nikonova</name></author><author><name sortKey="Loskutov, Yv" uniqKey="Loskutov Y">YV Loskutov</name></author><author><name sortKey="Kozyulina, Py" uniqKey="Kozyulina P">PY Kozyulina</name></author><author><name sortKey="Pugacheva, En" uniqKey="Pugacheva E">EN Pugacheva</name></author><author><name sortKey="Golemis, Ea" uniqKey="Golemis E">EA Golemis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Plotnikova, Ov" uniqKey="Plotnikova O">OV Plotnikova</name></author><author><name sortKey="Pugacheva, En" uniqKey="Pugacheva E">EN Pugacheva</name></author><author><name sortKey="Golemis, Ea" uniqKey="Golemis E">EA Golemis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Pugacheva, En" uniqKey="Pugacheva E">EN Pugacheva</name></author><author><name sortKey="Jablonski, Sa" uniqKey="Jablonski S">SA Jablonski</name></author><author><name sortKey="Hartman, Tr" uniqKey="Hartman T">TR Hartman</name></author><author><name sortKey="Henske, Ep" uniqKey="Henske E">EP Henske</name></author><author><name sortKey="Golemis, Ea" uniqKey="Golemis E">EA Golemis</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ritter, A" uniqKey="Ritter A">A Ritter</name></author><author><name sortKey="Friemel, A" uniqKey="Friemel A">A Friemel</name></author><author><name sortKey="Kreis, Nn" uniqKey="Kreis N">NN Kreis</name></author><author><name sortKey="Hoock, Sc" uniqKey="Hoock S">SC Hoock</name></author><author><name sortKey="Roth, S" uniqKey="Roth S">S Roth</name></author><author><name sortKey="Kielland Kaisen, U" uniqKey="Kielland Kaisen U">U Kielland-Kaisen</name></author><author><name sortKey="Bruggmann, D" uniqKey="Bruggmann D">D Bruggmann</name></author><author><name sortKey="Solbach, C" uniqKey="Solbach C">C Solbach</name></author><author><name sortKey="Louwen, F" uniqKey="Louwen F">F Louwen</name></author><author><name sortKey="Yuan, J" uniqKey="Yuan J">J Yuan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Seeley, Es" uniqKey="Seeley E">ES Seeley</name></author><author><name sortKey="Carriere, C" uniqKey="Carriere C">C Carriere</name></author><author><name sortKey="Goetze, T" uniqKey="Goetze T">T Goetze</name></author><author><name sortKey="Longnecker, Ds" uniqKey="Longnecker D">DS Longnecker</name></author><author><name sortKey="Korc, M" uniqKey="Korc M">M Korc</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Seeley, Es" uniqKey="Seeley E">ES Seeley</name></author><author><name sortKey="Carriere, C" uniqKey="Carriere C">C Carriere</name></author><author><name sortKey="Goetze, T" uniqKey="Goetze T">T Goetze</name></author><author><name sortKey="Longnecker, Ds" uniqKey="Longnecker D">DS Longnecker</name></author><author><name sortKey="Korc, M" uniqKey="Korc M">M Korc</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Servattalab, S" uniqKey="Servattalab S">S Servattalab</name></author><author><name sortKey="Yildiz, O" uniqKey="Yildiz O">O Yildiz</name></author><author><name sortKey="Khanna, H" uniqKey="Khanna H">H Khanna</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shin, Jh" uniqKey="Shin J">JH Shin</name></author><author><name sortKey="Bae, Dj" uniqKey="Bae D">DJ Bae</name></author><author><name sortKey="Kim, Es" uniqKey="Kim E">ES Kim</name></author><author><name sortKey="Kim, Hb" uniqKey="Kim H">HB Kim</name></author><author><name sortKey="Park, Sj" uniqKey="Park S">SJ Park</name></author><author><name sortKey="Jo, Yk" uniqKey="Jo Y">YK Jo</name></author><author><name sortKey="Jo, Ds" uniqKey="Jo D">DS Jo</name></author><author><name sortKey="Jo, Dg" uniqKey="Jo D">DG Jo</name></author><author><name sortKey="Kim, Sy" uniqKey="Kim S">SY Kim</name></author><author><name sortKey="Cho, Dh" uniqKey="Cho D">DH Cho</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shin, Jh" uniqKey="Shin J">JH Shin</name></author><author><name sortKey="Kim, Ps" uniqKey="Kim P">PS Kim</name></author><author><name sortKey="Kim, Es" uniqKey="Kim E">ES Kim</name></author><author><name sortKey="Park, Sj" uniqKey="Park S">SJ Park</name></author><author><name sortKey="Jo, Yk" uniqKey="Jo Y">YK Jo</name></author><author><name sortKey="Hwang, Jj" uniqKey="Hwang J">JJ Hwang</name></author><author><name sortKey="Park, Tj" uniqKey="Park T">TJ Park</name></author><author><name sortKey="Chang, Jw" uniqKey="Chang J">JW Chang</name></author><author><name sortKey="Seo, Jh" uniqKey="Seo J">JH Seo</name></author><author><name sortKey="Cho, Dh" uniqKey="Cho D">DH Cho</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Song, Dk" uniqKey="Song D">DK Song</name></author><author><name sortKey="Choi, Jh" uniqKey="Choi J">JH Choi</name></author><author><name sortKey="Kim, Ms" uniqKey="Kim M">MS Kim</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Stanley, Re" uniqKey="Stanley R">RE Stanley</name></author><author><name sortKey="Ragusa, Mj" uniqKey="Ragusa M">MJ Ragusa</name></author><author><name sortKey="Hurley, Jh" uniqKey="Hurley J">JH Hurley</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Struchtrup, A" uniqKey="Struchtrup A">A Struchtrup</name></author><author><name sortKey="Wiegering, A" uniqKey="Wiegering A">A Wiegering</name></author><author><name sortKey="Stork, B" uniqKey="Stork B">B Stork</name></author><author><name sortKey="Ruther, U" uniqKey="Ruther U">U Ruther</name></author><author><name sortKey="Gerhardt, C" uniqKey="Gerhardt C">C Gerhardt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Takahashi, K" uniqKey="Takahashi K">K Takahashi</name></author><author><name sortKey="Nagai, T" uniqKey="Nagai T">T Nagai</name></author><author><name sortKey="Chiba, S" uniqKey="Chiba S">S Chiba</name></author><author><name sortKey="Nakayama, K" uniqKey="Nakayama K">K Nakayama</name></author><author><name sortKey="Mizuno, K" uniqKey="Mizuno K">K Mizuno</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tang, Z" uniqKey="Tang Z">Z Tang</name></author><author><name sortKey="Lin, Mg" uniqKey="Lin M">MG Lin</name></author><author><name sortKey="Stowe, Tr" uniqKey="Stowe T">TR Stowe</name></author><author><name sortKey="Chen, S" uniqKey="Chen S">S Chen</name></author><author><name sortKey="Zhu, M" uniqKey="Zhu M">M Zhu</name></author><author><name sortKey="Stearns, T" uniqKey="Stearns T">T Stearns</name></author><author><name sortKey="Franco, B" uniqKey="Franco B">B Franco</name></author><author><name sortKey="Zhong, Q" uniqKey="Zhong Q">Q Zhong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Taschner, M" uniqKey="Taschner M">M Taschner</name></author><author><name sortKey="Bhogaraju, S" uniqKey="Bhogaraju S">S Bhogaraju</name></author><author><name sortKey="Lorentzen, E" uniqKey="Lorentzen E">E Lorentzen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Taylor, Sp" uniqKey="Taylor S">SP Taylor</name></author><author><name sortKey="Dantas, Tj" uniqKey="Dantas T">TJ Dantas</name></author><author><name sortKey="Duran, I" uniqKey="Duran I">I Duran</name></author><author><name sortKey="Wu, S" uniqKey="Wu S">S Wu</name></author><author><name sortKey="Lachman, Rs" uniqKey="Lachman R">RS Lachman</name></author><author><name sortKey="Nelson, Sf" uniqKey="Nelson S">SF Nelson</name></author><author><name sortKey="Cohn, Dh" uniqKey="Cohn D">DH Cohn</name></author><author><name sortKey="Vallee, Rb" uniqKey="Vallee R">RB Vallee</name></author><author><name sortKey="Krakow, D" uniqKey="Krakow D">D Krakow</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Tong, Y" uniqKey="Tong Y">Y Tong</name></author><author><name sortKey="Park, Sh" uniqKey="Park S">SH Park</name></author><author><name sortKey="Wu, D" uniqKey="Wu D">D Wu</name></author><author><name sortKey="Xu, W" uniqKey="Xu W">W Xu</name></author><author><name sortKey="Guillot, Sj" uniqKey="Guillot S">SJ Guillot</name></author><author><name sortKey="Jin, L" uniqKey="Jin L">L Jin</name></author><author><name sortKey="Li, X" uniqKey="Li X">X Li</name></author><author><name sortKey="Wang, Y" uniqKey="Wang Y">Y Wang</name></author><author><name sortKey="Lin, Cs" uniqKey="Lin C">CS Lin</name></author><author><name sortKey="Fu, Z" uniqKey="Fu Z">Z Fu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Volta, F" uniqKey="Volta F">F Volta</name></author><author><name sortKey="Gerdes, Jm" uniqKey="Gerdes J">JM Gerdes</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, S" uniqKey="Wang S">S Wang</name></author><author><name sortKey="Livingston, Mj" uniqKey="Livingston M">MJ Livingston</name></author><author><name sortKey="Su, Y" uniqKey="Su Y">Y Su</name></author><author><name sortKey="Dong, Z" uniqKey="Dong Z">Z Dong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wang, Zl" uniqKey="Wang Z">ZL Wang</name></author><author><name sortKey="Deng, Q" uniqKey="Deng Q">Q Deng</name></author><author><name sortKey="Chong, T" uniqKey="Chong T">T Chong</name></author><author><name sortKey="Wang, Zm" uniqKey="Wang Z">ZM Wang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wheway, G" uniqKey="Wheway G">G Wheway</name></author><author><name sortKey="Parry, Da" uniqKey="Parry D">DA Parry</name></author><author><name sortKey="Johnson, Ca" uniqKey="Johnson C">CA Johnson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="White, E" uniqKey="White E">E White</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wiegering, A" uniqKey="Wiegering A">A Wiegering</name></author><author><name sortKey="Ruther, U" uniqKey="Ruther U">U Ruther</name></author><author><name sortKey="Gerhardt, C" uniqKey="Gerhardt C">C Gerhardt</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xiao, Zs" uniqKey="Xiao Z">ZS Xiao</name></author><author><name sortKey="Quarles, Ld" uniqKey="Quarles L">LD Quarles</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, Q" uniqKey="Xu Q">Q Xu</name></author><author><name sortKey="Liu, W" uniqKey="Liu W">W Liu</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X Liu</name></author><author><name sortKey="Liu, W" uniqKey="Liu W">W Liu</name></author><author><name sortKey="Wang, H" uniqKey="Wang H">H Wang</name></author><author><name sortKey="Yao, G" uniqKey="Yao G">G Yao</name></author><author><name sortKey="Zang, L" uniqKey="Zang L">L Zang</name></author><author><name sortKey="Hayashi, T" uniqKey="Hayashi T">T Hayashi</name></author><author><name sortKey="Tashiro, S" uniqKey="Tashiro S">S Tashiro</name></author><author><name sortKey="Onodera, S" uniqKey="Onodera S">S Onodera</name></author><author><name sortKey="Ikejima, T" uniqKey="Ikejima T">T Ikejima</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Xu, Q" uniqKey="Xu Q">Q Xu</name></author><author><name sortKey="Liu, W" uniqKey="Liu W">W Liu</name></author><author><name sortKey="Liu, X" uniqKey="Liu X">X Liu</name></author><author><name sortKey="Otkur, W" uniqKey="Otkur W">W Otkur</name></author><author><name sortKey="Hayashi, T" uniqKey="Hayashi T">T Hayashi</name></author><author><name sortKey="Yamato, M" uniqKey="Yamato M">M Yamato</name></author><author><name sortKey="Fujisaki, H" uniqKey="Fujisaki H">H Fujisaki</name></author><author><name sortKey="Hattori, S" uniqKey="Hattori S">S Hattori</name></author><author><name sortKey="Tashiro, Si" uniqKey="Tashiro S">SI Tashiro</name></author><author><name sortKey="Ikejima, T" uniqKey="Ikejima T">T Ikejima</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yang, Sh" uniqKey="Yang S">SH Yang</name></author><author><name sortKey="Wang, Xx" uniqKey="Wang X">XX Wang</name></author><author><name sortKey="Contino, G" uniqKey="Contino G">G Contino</name></author><author><name sortKey="Liesa, M" uniqKey="Liesa M">M Liesa</name></author><author><name sortKey="Sahin, E" uniqKey="Sahin E">E Sahin</name></author><author><name sortKey="Ying, Hq" uniqKey="Ying H">HQ Ying</name></author><author><name sortKey="Bause, A" uniqKey="Bause A">A Bause</name></author><author><name sortKey="Li, Yh" uniqKey="Li Y">YH Li</name></author><author><name sortKey="Stommel, Jm" uniqKey="Stommel J">JM Stommel</name></author><author><name sortKey="Dell Ntonio, G" uniqKey="Dell Ntonio G">G Dell’Antonio</name></author><author><name sortKey="Mautner, J" uniqKey="Mautner J">J Mautner</name></author><author><name sortKey="Tonon, G" uniqKey="Tonon G">G Tonon</name></author><author><name sortKey="Haigis, M" uniqKey="Haigis M">M Haigis</name></author><author><name sortKey="Shirihai, Os" uniqKey="Shirihai O">OS Shirihai</name></author><author><name sortKey="Doglioni, C" uniqKey="Doglioni C">C Doglioni</name></author><author><name sortKey="Bardeesy, N" uniqKey="Bardeesy N">N Bardeesy</name></author><author><name sortKey="Kimmelman, Ac" uniqKey="Kimmelman A">AC Kimmelman</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Youn, Yh" uniqKey="Youn Y">YH Youn</name></author><author><name sortKey="Han, Yg" uniqKey="Han Y">YG Han</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Yuan, K" uniqKey="Yuan K">K Yuan</name></author><author><name sortKey="Frolova, N" uniqKey="Frolova N">N Frolova</name></author><author><name sortKey="Xie, Y" uniqKey="Xie Y">Y Xie</name></author><author><name sortKey="Wang, D" uniqKey="Wang D">D Wang</name></author><author><name sortKey="Cook, L" uniqKey="Cook L">L Cook</name></author><author><name sortKey="Kwon, Yj" uniqKey="Kwon Y">YJ Kwon</name></author><author><name sortKey="Steg, Ad" uniqKey="Steg A">AD Steg</name></author><author><name sortKey="Serra, R" uniqKey="Serra R">R Serra</name></author><author><name sortKey="Frost, Ar" uniqKey="Frost A">AR Frost</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhao, Yg" uniqKey="Zhao Y">YG Zhao</name></author><author><name sortKey="Zhang, H" uniqKey="Zhang H">H Zhang</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhi, X" uniqKey="Zhi X">X Zhi</name></author><author><name sortKey="Zhong, Q" uniqKey="Zhong Q">Q Zhong</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zingg, D" uniqKey="Zingg D">D Zingg</name></author><author><name sortKey="Debbache, J" uniqKey="Debbache J">J Debbache</name></author><author><name sortKey="Pena Hernandez, R" uniqKey="Pena Hernandez R">R Pena-Hernandez</name></author><author><name sortKey="Antunes, At" uniqKey="Antunes A">AT Antunes</name></author><author><name sortKey="Schaefer, Sm" uniqKey="Schaefer S">SM Schaefer</name></author><author><name sortKey="Cheng, Pf" uniqKey="Cheng P">PF Cheng</name></author><author><name sortKey="Zimmerli, D" uniqKey="Zimmerli D">D Zimmerli</name></author><author><name sortKey="Haeusel, J" uniqKey="Haeusel J">J Haeusel</name></author><author><name sortKey="Calcada, Rr" uniqKey="Calcada R">RR Calcada</name></author><author><name sortKey="Tuncer, E" uniqKey="Tuncer E">E Tuncer</name></author><author><name sortKey="Zhang, Y" uniqKey="Zhang Y">Y Zhang</name></author><author><name sortKey="Bossart, R" uniqKey="Bossart R">R Bossart</name></author><author><name sortKey="Wong, Kk" uniqKey="Wong K">KK Wong</name></author><author><name sortKey="Basler, K" uniqKey="Basler K">K Basler</name></author><author><name sortKey="Dummer, R" uniqKey="Dummer R">R Dummer</name></author><author><name sortKey="Santoro, R" uniqKey="Santoro R">R Santoro</name></author><author><name sortKey="Levesque, Mp" uniqKey="Levesque M">MP Levesque</name></author><author><name sortKey="Sommer, L" uniqKey="Sommer L">L Sommer</name></author></analytic></biblStruct></listBibl></div1></back></TEI><pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Biomol Ther (Seoul)</journal-id><journal-id journal-id-type="iso-abbrev">Biomol Ther (Seoul)</journal-id><journal-id journal-id-type="publisher-id">Biomol Ther (Seoul)</journal-id><journal-id journal-id-type="publisher-id">ksp</journal-id><journal-title-group><journal-title>Biomolecules & Therapeutics</journal-title></journal-title-group><issn pub-type="ppub">1976-9148</issn><issn pub-type="epub">2005-4483</issn><publisher><publisher-name>The Korean Society of Applied Pharmacology</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31042678</article-id><article-id pub-id-type="pmc">6609109</article-id><article-id pub-id-type="doi">10.4062/biomolther.2019.056</article-id><article-id pub-id-type="publisher-id">bt-27-337</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Interplay Between Primary Cilia and Autophagy and Its Controversial Roles in Cancer</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Ko</surname><given-names>Je Yeong</given-names></name><xref ref-type="author-notes" rid="fn1-bt-27-337"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Lee</surname><given-names>Eun Ji</given-names></name><xref ref-type="author-notes" rid="fn1-bt-27-337"><sup>†</sup></xref></contrib><contrib contrib-type="author"><name><surname>Park</surname><given-names>Jong Hoon</given-names></name><xref rid="c1-bt-27-337" ref-type="corresp"><sup>*</sup></xref></contrib><aff id="af1-bt-27-337">Department of Life Systems, Sookmyung Women’s University, Seoul 04310,<country>Republic of Korea</country></aff></contrib-group><author-notes><fn id="fn1-bt-27-337" fn-type="equal"><label>†</label><p>The first two authors contributed equally to this work.</p></fn><corresp id="c1-bt-27-337"><label>*</label>Corresponding Author: E-mail: <email>parkjh@sookmyung.ac.kr</email>, Tel: +82-2-710-9414, Fax: +82-2-2077-7258</corresp></author-notes><pub-date pub-type="ppub"><month>7</month><year>2019</year></pub-date><pub-date pub-type="epub"><day>02</day><month>5</month><year>2019</year></pub-date><volume>27</volume><issue>4</issue><fpage>337</fpage><lpage>341</lpage><history><date date-type="received"><day>29</day><month>3</month><year>2019</year></date><date date-type="rev-recd"><day>03</day><month>4</month><year>2019</year></date><date date-type="accepted"><day>05</day><month>4</month><year>2019</year></date></history><permissions><copyright-statement>Copyright ©2019, The Korean Society of Applied Pharmacology</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/"><license-p><pmc-comment>CREATIVE COMMONS</pmc-comment>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/4.0/">http://creativecommons.org/licenses/by-nc/4.0/</ext-link>) which per mits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>Primary cilia and autophagy are two distinct nutrient-sensing machineries required for maintaining intracellular energy homeostasis, either via signal transduction or recycling of macromolecules from cargo breakdown, respectively. Potential correlations between primary cilia and autophagy have been recently suggested and their relationship may increase our understanding of the pathogenesis of human diseases, including ciliopathies and cancer. In this review, we cover the current issues concerning the bidirectional interaction between primary cilia and autophagy and discuss its role in cancer with cilia defect.</p></abstract><kwd-group><kwd>Cilia</kwd><kwd>Autophagy</kwd><kwd>Ciliopathy</kwd><kwd>Cancer</kwd></kwd-group></article-meta></front><body><sec sec-type="intro"><title>INTRODUCTION</title><p>Primary cilia are nonmotile, antenna-like organelles derived from the centrioles after cell division, and are therefore closely related to cell cycle control. These structure sense extracellular stimuli, including growth factors and mechanical stress, via multiple receptors clustered along the ciliary membrane. They are also known to contribute to metabolic regulation (<xref rid="b11-bt-27-337" ref-type="bibr">Delaine-Smith <italic>et al</italic>., 2014</xref>). Autophagy is an intracellular process required for maintaining energy homeostasis, whereby damaged proteins are removed and recycled. This process is generally inhibited by the energy-sensing mTORC1 (mammalian target of rapamycin complex 1) under fed conditions, and is triggered by cellular stresses, including serum deprivation (<xref rid="b12-bt-27-337" ref-type="bibr">Glick <italic>et al</italic>., 2010</xref>).</p><p>Potential correlations between primary cilia and autophagy have been recently suggested and an increasing number of studies are attempting to identify its specific molecular mechanisms (<xref rid="b9-bt-27-337" ref-type="bibr">Cloonan <italic>et al</italic>., 2014</xref>; <xref rid="b34-bt-27-337" ref-type="bibr">Pampliega and Cuervo, 2016</xref>; <xref rid="b3-bt-27-337" ref-type="bibr">Avalos <italic>et al</italic>., 2017</xref>). Herein, we summarize the current issues regarding the bidirectional interplay between ciliogenesis and autophagy, and discuss its pathophysiological implications.</p></sec><sec sec-type="other"><title>PRIMARY CILIA</title><p>Primary cilia are finger-like organelles protruding from the apical membrane of many mammalian cells. Non-motile primary cilia were considered to be ancient cellular organelles that lack a specific biological function. However, recent studies have reported that various signaling proteins and channels are localized to ciliary membranes and respond to diverse stimuli such as mechanical stress (<xref rid="b11-bt-27-337" ref-type="bibr">Delaine-Smith <italic>et al</italic>., 2014</xref>; <xref rid="b6-bt-27-337" ref-type="bibr">Battle <italic>et al</italic>., 2015</xref>) and various signaling molecules from the extracellular environment (<xref rid="b26-bt-27-337" ref-type="bibr">Malicki and Johnson, 2017</xref>; <xref rid="b45-bt-27-337" ref-type="bibr">Song <italic>et al</italic>., 2018</xref>). The biological significance of primary cilia is exemplified by the fact that functional or structural defects in the primary cilia in mice results in pathological phenotypes known as ciliopathies, such as cystic disease (<xref rid="b16-bt-27-337" ref-type="bibr">Jonassen <italic>et al</italic>., 2008</xref>, <xref rid="b17-bt-27-337" ref-type="bibr">2012</xref>), cancer (<xref rid="b28-bt-27-337" ref-type="bibr">Menzl <italic>et al</italic>., 2014</xref>; <xref rid="b15-bt-27-337" ref-type="bibr">Jenks <italic>et al</italic>., 2018</xref>; <xref rid="b13-bt-27-337" ref-type="bibr">Higgins <italic>et al</italic>., 2019</xref>), obesity (<xref rid="b53-bt-27-337" ref-type="bibr">Volta and Gerdes, 2017</xref>; <xref rid="b39-bt-27-337" ref-type="bibr">Ritter <italic>et al</italic>., 2018</xref>), blindness (<xref rid="b42-bt-27-337" ref-type="bibr">Servattalab <italic>et al</italic>., 2012</xref>; <xref rid="b56-bt-27-337" ref-type="bibr">Wheway <italic>et al</italic>., 2014</xref>), polydactyly (<xref rid="b51-bt-27-337" ref-type="bibr">Taylor <italic>et al</italic>., 2015</xref>; <xref rid="b1-bt-27-337" ref-type="bibr">Agbu <italic>et al</italic>., 2018</xref>), left-right asymmetry defects (<xref rid="b33-bt-27-337" ref-type="bibr">Okada <italic>et al</italic>., 1999</xref>; <xref rid="b10-bt-27-337" ref-type="bibr">Dasgupta and Amack, 2016</xref>), skeletal abnormalities (<xref rid="b59-bt-27-337" ref-type="bibr">Xiao and Quarles, 2010</xref>), and neurological impairment (<xref rid="b63-bt-27-337" ref-type="bibr">Youn and Han, 2018</xref>). Based on this evidence, primary cilia have emerged as signaling hubs involved in the regulation of diverse cell signaling.</p><p>Primary cilia consist of dynamic microtubule-based axoneme regulated by a precise mechanism called ciliogenesis (<xref rid="b50-bt-27-337" ref-type="bibr">Taschner <italic>et al</italic>., 2012</xref>). Key proteins during ciliogenesis are the intraflagellar transport (IFT) particles, which are protein complexes that move bidirectionally along the ciliary axoneme (<xref rid="b50-bt-27-337" ref-type="bibr">Taschner <italic>et al</italic>., 2012</xref>; <xref rid="b23-bt-27-337" ref-type="bibr">Lechtreck, 2015</xref>). In addition to IFT complexes, cell cycle regulators are involved in ciliogenesis (<xref rid="b38-bt-27-337" ref-type="bibr">Pugacheva <italic>et al</italic>., 2007</xref>; <xref rid="b36-bt-27-337" ref-type="bibr">Plotnikova <italic>et al</italic>., 2012</xref>), with primary cilia typically assembling in response to quiescence (G1/G0 phase) and disassembling upon cell cycle re-entry (<xref rid="b37-bt-27-337" ref-type="bibr">Plotnikova <italic>et al</italic>., 2009</xref>; <xref rid="b4-bt-27-337" ref-type="bibr">Basten and Giles, 2013</xref>). Interestingly, multiple lines of research have revealed that autophagy (<xref rid="b49-bt-27-337" ref-type="bibr">Tang <italic>et al</italic>., 2013</xref>), the ubiquitin-proteasome system (<xref rid="b18-bt-27-337" ref-type="bibr">Kasahara <italic>et al</italic>., 2014</xref>), actin remodeling factors such as LIM kinase 2 (LIMK2), testicular protein kinase (TESK1) (<xref rid="b21-bt-27-337" ref-type="bibr">Kim <italic>et al</italic>., 2015b</xref>), and serine/threonine kinases such as intestinal cell kinase (ICK) (<xref rid="b8-bt-27-337" ref-type="bibr">Chaya <italic>et al</italic>., 2014</xref>; <xref rid="b30-bt-27-337" ref-type="bibr">Moon <italic>et al</italic>., 2014</xref>) are critical for the maintenance and function of primary cilia. More recently, among these various regulators of ciliogenesis or ciliary function, interest in the bidirectional interaction between primary cilia and autophagy is increasing (<xref rid="b34-bt-27-337" ref-type="bibr">Pampliega and Cuervo, 2016</xref>; <xref rid="b58-bt-27-337" ref-type="bibr">Wiegering <italic>et al</italic>., 2019</xref>). Indeed, it has been reported that cells with defective cilia show reduced autophagy (<xref rid="b35-bt-27-337" ref-type="bibr">Pampliega <italic>et al</italic>., 2013</xref>) and dysfunction of ICK known as ciliary protein leads to perturbation of ciliary signaling and autophagy (<xref rid="b52-bt-27-337" ref-type="bibr">Tong <italic>et al</italic>., 2017</xref>), which suggests that there is a close relationship between primary cilia and autophagy.</p></sec><sec sec-type="other"><title>AUTOPHAGY</title><p>Autophagy is a highly conserved intracellular process in which misfolded or damaged proteins are sequestered into double membrane-bound vesicles named autophagosomes. More than 30 autophagy-related (<italic>Atg</italic>) genes are sequentially involved in autophagosome formation, and once formed, these vesicles fuse with lysosomes so that their engulfed cargo can be degraded by hydrolytic enzymes. Autophagy eliminates harmful intracellular proteins and recycles the functional macromolecular components, helping to ensure the maintenance of cellular homeostasis (<xref rid="b12-bt-27-337" ref-type="bibr">Glick <italic>et al</italic>., 2010</xref>).</p><p>The stepwise process of autophagy is divided into four stages: initiation, vesicle nucleation, elongation of autophago-some, and fusion with a lysosome (<xref rid="b29-bt-27-337" ref-type="bibr">Mizushima <italic>et al</italic>., 2011</xref>; <xref rid="b46-bt-27-337" ref-type="bibr">Stanley <italic>et al</italic>., 2014</xref>). It initially starts with the accumulation of the ULK1/2 (Unc-51 like autophagy activating kinase 1/2) complex (ULK1/2-ATG13-FIP200), which is normally inhibited by the energy-sensing mTORC1 under fed conditions. mTORC1 inactivation, under autophagy-related stimuli including nutrient deprivation, in turn de-phosphorylates ULK1/2 and ATG13 and enhances the interaction between them. The active ULK1/2 complex translocates to cytosolic membrane structures where the phagophore membrane is possibly derived (<xref rid="b2-bt-27-337" ref-type="bibr">Alers <italic>et al</italic>., 2012</xref>). Beclin 1, which is phosphorylated by ULK1, is one of the core proteins that initiate vesicle nucleation. It forms a complex with VPS34 (phosphatidylinositol 3-kinase catalytic subunit type 3) and subsequently interacts with co-activators (i.e., Vps15, UVRAG (UV radiation resistance associated gene) and Bif-1 (SH3 domain containing GRB2 like, endophilin B1)) to generate phosphatidylinositol-3-phosphate (Ptdlns3P), which recruits other ATG proteins to grow the autophagosomal membrane from the phagophore (<xref rid="b19-bt-27-337" ref-type="bibr">Kihara <italic>et al</italic>., 2001</xref>). During vesicle elongation, the microtubule-associated protein 1A/1B-light chain 3 (LC3) is processed to an active lipid-conjugated form, which allows for its incorporation into the autophagosomal membrane. Specific ATG proteins including ATG3, ATG4, the ATG5/ATG12/ATG16L complex, and ATG7 are sequentially involved in this stage (<xref rid="b31-bt-27-337" ref-type="bibr">Nakatogawa <italic>et al</italic>., 2007</xref>). As the autophagosome becomes enclosed and completely matured, it fuses with lysosomes, which then allows for the proteolytic degradation of engulfed cargo proteins (<xref rid="b65-bt-27-337" ref-type="bibr">Zhao and Zhang, 2019</xref>).</p></sec><sec sec-type="other"><title>INTERPLAY BETWEEN AUTOPHAGY AND PRIMARY CILIA</title><p>Autophagy and ciliogenesis occur concurrently under serum deprivation and both are involved in maintaining intracellular energy balance, which suggests that the two might be linked. The first two studies identifying interplay between autophagy and ciliogenesis were published in 2013. One study found that autophagy regulated a cilia-related protein Oral-facial-digital syndrome 1 protein (OFD1, centriole and centriolar satellite protein). The authors identified that a centriolar satellite protein OFD1 negatively regulates ciliogenesis, and under fasted conditions, autophagy eliminates it (<xref rid="b49-bt-27-337" ref-type="bibr">Tang <italic>et al</italic>., 2013</xref>) (<xref rid="f1-bt-27-337" ref-type="fig">Fig. 1A</xref>). The second study showed that impaired autophagic flux as well as reduced ciliogenesis occurred following serum withdrawal in cilia-defect models. In addition, a large number of ATG proteins turned out to be localized either to the basal body, where a cilium is primarily nucleated, or along the ciliary axoneme, suggesting a potential cilia-mediated autophagy initiation mechanism (<xref rid="b35-bt-27-337" ref-type="bibr">Pampliega <italic>et al</italic>., 2013</xref>). Studies to further identify the functional relationship between autophagy and ciliogenesis are currently underway.</p><p>Early approaches attempted to determine whether the two processes were concurrently triggered following a common stimulus, and whether they influenced each other. Bidirectional regulation between autophagy and cilia was indeed observed, with impaired autophagic flux in cells with cilia defects as well as shorter cilia led by autophagy inhibition (<xref rid="b54-bt-27-337" ref-type="bibr">Wang <italic>et al</italic>., 2015</xref>). Several studies also demonstrated either genetic or chemical inhibition of autophagy attenuated cilia growth that was stimulated by chemicals including Sertraline, BIX01294, and Mefloquine in retinal pigment epithelium (RPE) cells (<xref rid="b20-bt-27-337" ref-type="bibr">Kim <italic>et al</italic>., 2015a</xref>; <xref rid="b43-bt-27-337" ref-type="bibr">Shin <italic>et al</italic>., 2015a</xref>, <xref rid="b44-bt-27-337" ref-type="bibr">2015b</xref>). These studies demonstrated positive correlations between autophagy and cilia growth; however, other studies have made contradictory findings. Using mouse embryo fibroblast 3T3-L1 cells, cilia were shortened by histone deacetylase 6 (HDAC6)-mediated autophagy via decreasing the expression of ciliary proteins such as IFTs and KIF3a (kinesin family member 3A) (<xref rid="b60-bt-27-337" ref-type="bibr">Xu <italic>et al</italic>., 2016</xref>). Similarly, downregulation of the HDAC6-autophagy pathway was involved in cilia growth promoted by type I collagen, which provides mechanical strength to modulate cellular morphology or shape (<xref rid="b61-bt-27-337" ref-type="bibr">Xu <italic>et al</italic>., 2018</xref>). More recently, studies to identify specific mediators regulating the autophagy-ciliogenesis axis were attempted. PPARA (peroxisome proliferator activated receptor alpha) was identified as one of these potential meditators, as it was found to positively regulate ciliogenesis, which was changed by drugs or genetic manipulations that targeted autophagy. <italic>In vivo</italic> data showing impaired autophagy as well as kidney damage, commonly observed in ciliopathies, in <italic>Ppara</italic><sup>−/−</sup> mice was further evidence for the involvement of autophagy in ciliogenesis (<xref rid="b25-bt-27-337" ref-type="bibr">Liu <italic>et al</italic>., 2018</xref>). In addition, another group suggested Gli2 as a link between primary cilia-dependent cell cycle control and autophagy, in which Gli2 repressed Ofd1-eliminating autophagy under serum deprivation (<xref rid="b14-bt-27-337" ref-type="bibr">Hsiao <italic>et al</italic>., 2018</xref>).</p><p>Taken together, these studies indicate that there is a substantial link between autophagy and ciliogenesis, in which impaired autophagy leads to a ciliary defect and vice versa. However, further studies are still required to identify the specific molecular mechanisms.</p></sec><sec sec-type="other"><title>CONTROVERSIAL INTERPLAY BETWEEN PRIMARY CILIA AND AUTOPHAGY IN CANCER</title><p>Multiple human cancers, including melanoma (<xref rid="b67-bt-27-337" ref-type="bibr">Zingg <italic>et al</italic>., 2018</xref>), renal cell carcinoma (<xref rid="b5-bt-27-337" ref-type="bibr">Basten <italic>et al</italic>., 2013</xref>), pancreatic cancer (<xref rid="b40-bt-27-337" ref-type="bibr">Seeley <italic>et al</italic>., 2009a</xref>; <xref rid="b22-bt-27-337" ref-type="bibr">Kobayashi and Itoh, 2017</xref>), and breast cancer (<xref rid="b28-bt-27-337" ref-type="bibr">Menzl <italic>et al</italic>., 2014</xref>; <xref rid="b32-bt-27-337" ref-type="bibr">Nobutani <italic>et al</italic>., 2014</xref>), are accompanied by primary ciliary defects (<xref rid="b64-bt-27-337" ref-type="bibr">Yuan <italic>et al</italic>., 2010</xref>) and dysregulated autophagy (<xref rid="b55-bt-27-337" ref-type="bibr">Wang <italic>et al</italic>., 2018</xref>). The relationship between primary cilia and autophagy still requires further studies; however, primary cilia are generally known to have a positive effect on autophagy regulation (<xref rid="b35-bt-27-337" ref-type="bibr">Pampliega <italic>et al</italic>., 2013</xref>; <xref rid="b54-bt-27-337" ref-type="bibr">Wang <italic>et al</italic>., 2015</xref>) (<xref rid="f1-bt-27-337" ref-type="fig">Fig. 1A</xref>). If this is true, how is autophagy regulated in cilia-deficient cancer models and what are the effects of autophagy regulators in cilia-defective cancer models?</p><p>It can be speculated that most cancer cells that do not have primary cilia have lower autophagic activity. Indeed, autophagy was suppressed in renal cell carcinoma (RCC) cell lines (<xref rid="b55-bt-27-337" ref-type="bibr">Wang <italic>et al</italic>., 2018</xref>) with decreased ciliated frequency (<xref rid="b5-bt-27-337" ref-type="bibr">Basten <italic>et al</italic>., 2013</xref>). However, many research groups have reported that autophagy has a dual function as both a tumor suppressor and tumor promoter, depending on the cancer subtype and development/progression stage (<xref rid="b57-bt-27-337" ref-type="bibr">White, 2015</xref>; <xref rid="b66-bt-27-337" ref-type="bibr">Zhi and Zhong, 2015</xref>). In this context, it is interesting that many cancer cells do not have primary cilia and yet they display differences in their autophagic activities, which indicates that the correlation between primary cilia and autophagy is still unclear in these cancer models. An example of this comes from a study where the effect of autophagy repression on cancer cells was investigated. In that study chloroquine (CQ), an inhibitor of late stage of autophagy (<xref rid="b27-bt-27-337" ref-type="bibr">Mauthe <italic>et al</italic>., 2018</xref>), was used in various human cancer models. Among these cancers, the pancreatic ductal adenocarcinoma (PDAC) cell line and its primary tumor display increased autophagic activities (<xref rid="b62-bt-27-337" ref-type="bibr">Yang <italic>et al</italic>., 2011</xref>) despite the absence of primary cilia (<xref rid="f1-bt-27-337" ref-type="fig">Fig. 1B</xref>) (<xref rid="b41-bt-27-337" ref-type="bibr">Seeley <italic>et al</italic>., 2009b</xref>; <xref rid="b22-bt-27-337" ref-type="bibr">Kobayashi and Itoh, 2017</xref>). Thus, even though primary cilia are suspected to have a positive effect on autophagy, the PDAC model indicates that there must be a cilia-independent mechanism for autophagy regulation (<xref rid="f1-bt-27-337" ref-type="fig">Fig. 1B</xref>). In the study with the PDAC cell lines, CQ treatment reduced growth and tumorigenesis (<xref rid="b62-bt-27-337" ref-type="bibr">Yang <italic>et al</italic>., 2011</xref>), suggesting that even if cancer cells do not have primary cilia, autophagy inhibition can show some anti-cancer effects (<xref rid="f1-bt-27-337" ref-type="fig">Fig. 1B</xref>). In addition to study of PDAC model, there is another research showing this controversial interplay in thyroid cancer (<xref rid="b24-bt-27-337" ref-type="bibr">Lee <italic>et al</italic>., 2016</xref>). XTC. UC1 cells derived from thyroid Hürthle cell carcinoma show higher activity of autophagy even though these cells display decreased frequency of ciliated cells compared with that in controls (<xref rid="f1-bt-27-337" ref-type="fig">Fig. 1C</xref>) (<xref rid="b24-bt-27-337" ref-type="bibr">Lee <italic>et al</italic>., 2016</xref>). Interestingly, pharmacological inhibition of autophagosome formation of XTC.UC1 cells using 3-MA treatment increases ciliogenesis via restoring expression of ciliary proteins, IFT88 and ARL13B (<xref rid="f1-bt-27-337" ref-type="fig">Fig. 1C</xref>) (<xref rid="b24-bt-27-337" ref-type="bibr">Lee <italic>et al</italic>., 2016</xref>). Likewise, cilia and autophagy seem to be related to each other in cancer, but may not be applied to cancer models with positive correlation observed in normal cells. Therefore, further studies are needed to reveal underlying regulatory mechanism between primary cilia and autophagy in various cancer models.</p></sec><sec sec-type="conclusions"><title>CONCLUSIONS</title><p>In the last few years, the interplay between primary cilia and autophagy has been an active area of research (<xref rid="b14-bt-27-337" ref-type="bibr">Hsiao <italic>et al</italic>., 2018</xref>; <xref rid="b47-bt-27-337" ref-type="bibr">Struchtrup <italic>et al</italic>., 2018</xref>; <xref rid="b48-bt-27-337" ref-type="bibr">Takahashi <italic>et al</italic>., 2018</xref>), and several studies have indicated that there is biological interaction between these two entities. Because primary cilia and autophagy have various cellular functions (<xref rid="b7-bt-27-337" ref-type="bibr">Cao and Zhong, 2015</xref>), the interaction of these two regulatory mechanism will provide critical evidences to help understand disease pathogenesis. However, the functional significance of primary cilia on autophagy and vice versa remains controversial. There is a bidirectional interplay between primary cilia and autophagy, but more studies are needed to explain this complicated connection. This is especially true in more complex diseases models such as cancer, where the interplay between primary cilia and autophagy is not as clear. Further studies are needed to investigate the regulatory mechanism between primary cilia and autophagy in disease models, as they may provide new therapeutic approaches of ciliopathies, including cancer.</p></sec></body><back><ack><p>This study was supported by a grant from the National Research Foundation of Korea (NRF) funded by the Korean government (MSIP) (2016R1A6A3A11932842, 2016R1A2A1A050 05295, 2016R1A5A1011974).</p></ack><ref-list><title>REFERENCES</title><ref id="b1-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Agbu</surname><given-names>SO</given-names></name><name><surname>Liang</surname><given-names>Y</given-names></name><name><surname>Liu</surname><given-names>A</given-names></name><name><surname>Anderson</surname><given-names>KV</given-names></name></person-group><year>2018</year><article-title>The small GTPase RSG1 controls a final step in primary cilia initiation</article-title><source>J Cell Biol</source><volume>217</volume><fpage>413</fpage><lpage>427</lpage><pub-id pub-id-type="doi">10.1083/jcb.201604048</pub-id><pmc-comment>5748968 </pmc-comment>
<pub-id pub-id-type="pmid">29038301</pub-id></element-citation></ref><ref id="b2-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Alers</surname><given-names>S</given-names></name><name><surname>Loffler</surname><given-names>AS</given-names></name><name><surname>Wesselborg</surname><given-names>S</given-names></name><name><surname>Stork</surname><given-names>B</given-names></name></person-group><year>2012</year><article-title>Role of AMPK-mTOR-Ulk1/2 in the regulation of autophagy: cross talk, shortcuts, and feedbacks</article-title><source>Mol Cell Biol</source><volume>32</volume><fpage>2</fpage><lpage>11</lpage><pub-id pub-id-type="doi">10.1128/MCB.06159-11</pub-id><pmc-comment>3255710 </pmc-comment>
<pub-id pub-id-type="pmid">22025673</pub-id></element-citation></ref><ref id="b3-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Avalos</surname><given-names>Y</given-names></name><name><surname>Pena-Oyarzun</surname><given-names>D</given-names></name><name><surname>Budini</surname><given-names>M</given-names></name><name><surname>Morselli</surname><given-names>E</given-names></name><name><surname>Criollo</surname><given-names>A</given-names></name></person-group><year>2017</year><article-title>New roles of the primary cilium in autophagy</article-title><source>Biomed Res Int</source><volume>2017</volume><fpage>4367019</fpage><pub-id pub-id-type="doi">10.1155/2017/4367019</pub-id><pmc-comment>5587941 </pmc-comment>
<pub-id pub-id-type="pmid">28913352</pub-id></element-citation></ref><ref id="b4-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Basten</surname><given-names>SG</given-names></name><name><surname>Giles</surname><given-names>RH</given-names></name></person-group><year>2013</year><article-title>Functional aspects of primary cilia in signaling, cell cycle and tumorigenesis</article-title><source>Cilia</source><volume>2</volume><fpage>6</fpage><pub-id pub-id-type="doi">10.1186/2046-2530-2-6</pub-id><pmc-comment>3662159 </pmc-comment>
<pub-id pub-id-type="pmid">23628112</pub-id></element-citation></ref><ref id="b5-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Basten</surname><given-names>SG</given-names></name><name><surname>Willekers</surname><given-names>S</given-names></name><name><surname>Vermaat</surname><given-names>JS</given-names></name><name><surname>Slaats</surname><given-names>GG</given-names></name><name><surname>Voest</surname><given-names>EE</given-names></name><name><surname>van Diest</surname><given-names>PJ</given-names></name><name><surname>Giles</surname><given-names>RH</given-names></name></person-group><year>2013</year><article-title>Reduced cilia frequencies in human renal cell carcinomas versus neighboring parenchymal tissue</article-title><source>Cilia</source><volume>2</volume><fpage>2</fpage><pub-id pub-id-type="doi">10.1186/2046-2530-2-2</pub-id><pmc-comment>3564780 </pmc-comment>
<pub-id pub-id-type="pmid">23369289</pub-id></element-citation></ref><ref id="b6-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Battle</surname><given-names>C</given-names></name><name><surname>Ott</surname><given-names>CM</given-names></name><name><surname>Burnette</surname><given-names>DT</given-names></name><name><surname>Lippincott-Schwartz</surname><given-names>J</given-names></name><name><surname>Schmidt</surname><given-names>CF</given-names></name></person-group><year>2015</year><article-title>Intracellular and extracellular forces drive primary cilia movement</article-title><source>Proc Natl Acad Sci USA</source><volume>112</volume><fpage>1410</fpage><lpage>1415</lpage><pub-id pub-id-type="doi">10.1073/pnas.1421845112</pub-id><pmc-comment>4321243 </pmc-comment>
<pub-id pub-id-type="pmid">25605896</pub-id></element-citation></ref><ref id="b7-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cao</surname><given-names>M</given-names></name><name><surname>Zhong</surname><given-names>Q</given-names></name></person-group><year>2015</year><article-title>Cilia in autophagy and cancer</article-title><source>Cilia</source><volume>5</volume><fpage>4</fpage><pub-id pub-id-type="doi">10.1186/s13630-016-0027-3</pub-id><pub-id pub-id-type="pmid">26848389</pub-id></element-citation></ref><ref id="b8-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Chaya</surname><given-names>T</given-names></name><name><surname>Omori</surname><given-names>Y</given-names></name><name><surname>Kuwahara</surname><given-names>R</given-names></name><name><surname>Furukawa</surname><given-names>T</given-names></name></person-group><year>2014</year><article-title>ICK is essential for cell type-specific ciliogenesis and the regulation of ciliary transport</article-title><source>EMBO J</source><volume>33</volume><fpage>1227</fpage><lpage>1242</lpage><pmc-comment>4198026 </pmc-comment>
<pub-id pub-id-type="pmid">24797473</pub-id></element-citation></ref><ref id="b9-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Cloonan</surname><given-names>SM</given-names></name><name><surname>Lam</surname><given-names>HC</given-names></name><name><surname>Ryter</surname><given-names>SW</given-names></name><name><surname>Choi</surname><given-names>AM</given-names></name></person-group><year>2014</year><article-title>“Ciliophagy”: the consumption of cilia components by autophagy</article-title><source>Autophagy</source><volume>10</volume><fpage>532</fpage><lpage>534</lpage><pub-id pub-id-type="doi">10.4161/auto.27641</pub-id><pmc-comment>4077895 </pmc-comment>
<pub-id pub-id-type="pmid">24401596</pub-id></element-citation></ref><ref id="b10-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Dasgupta</surname><given-names>A</given-names></name><name><surname>Amack</surname><given-names>JD</given-names></name></person-group><year>2016</year><article-title>Cilia in vertebrate left-right patterning</article-title><source>Philos. Trans. R. Soc. Lond., B, Biol Sci</source><volume>371</volume><fpage>20150410</fpage><pub-id pub-id-type="doi">10.1098/rstb.2015.0410</pub-id><pmc-comment>5104509 </pmc-comment>
<pub-id pub-id-type="pmid">27821522</pub-id></element-citation></ref><ref id="b11-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Delaine-Smith</surname><given-names>RM</given-names></name><name><surname>Sittichokechaiwut</surname><given-names>A</given-names></name><name><surname>Reilly</surname><given-names>GC</given-names></name></person-group><year>2014</year><article-title>Primary cilia respond to fluid shear stress and mediate flow-induced calcium deposition in osteoblasts</article-title><source>FASEB J</source><volume>28</volume><fpage>430</fpage><lpage>439</lpage><pub-id pub-id-type="doi">10.1096/fj.13-231894</pub-id><pmc-comment>4012163 </pmc-comment>
<pub-id pub-id-type="pmid">24097311</pub-id></element-citation></ref><ref id="b12-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Glick</surname><given-names>D</given-names></name><name><surname>Barth</surname><given-names>S</given-names></name><name><surname>Macleod</surname><given-names>KF</given-names></name></person-group><year>2010</year><article-title>Autophagy: cellular and molecular mechanisms</article-title><source>J Pathol</source><volume>221</volume><fpage>3</fpage><lpage>12</lpage><pub-id pub-id-type="doi">10.1002/path.2697</pub-id><pmc-comment>2990190 </pmc-comment>
<pub-id pub-id-type="pmid">20225336</pub-id></element-citation></ref><ref id="b13-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Higgins</surname><given-names>M</given-names></name><name><surname>Obaidi</surname><given-names>I</given-names></name><name><surname>McMorrow</surname><given-names>T</given-names></name></person-group><year>2019</year><article-title>Primary cilia and their role in cancer</article-title><source>Oncol Lett</source><volume>17</volume><fpage>3041</fpage><lpage>3047</lpage><pmc-comment>6396132 </pmc-comment>
<pub-id pub-id-type="pmid">30867732</pub-id></element-citation></ref><ref id="b14-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Hsiao</surname><given-names>CJ</given-names></name><name><surname>Chang</surname><given-names>CH</given-names></name><name><surname>Ibrahim</surname><given-names>RB</given-names></name><name><surname>Lin</surname><given-names>IH</given-names></name><name><surname>Wang</surname><given-names>CH</given-names></name><name><surname>Wang</surname><given-names>WJ</given-names></name><name><surname>Tsai</surname><given-names>JW</given-names></name></person-group><year>2018</year><article-title>Gli2 modulates cell cycle re-entry through autophagy-mediated regulation of the length of primary cilia</article-title><source>J. Cell Sci</source><volume>131</volume><fpage>jcs221218</fpage><pub-id pub-id-type="doi">10.1242/jcs.221218</pub-id><pub-id pub-id-type="pmid">30463852</pub-id></element-citation></ref><ref id="b15-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jenks</surname><given-names>AD</given-names></name><name><surname>Vyse</surname><given-names>S</given-names></name><name><surname>Wong</surname><given-names>JP</given-names></name><name><surname>Kostaras</surname><given-names>E</given-names></name><name><surname>Keller</surname><given-names>D</given-names></name><name><surname>Burgoyne</surname><given-names>T</given-names></name><name><surname>Shoemark</surname><given-names>A</given-names></name><name><surname>Tsalikis</surname><given-names>A</given-names></name><name><surname>de la Roche</surname><given-names>M</given-names></name><name><surname>Michaelis</surname><given-names>M</given-names></name><name><surname>Cinatl</surname><given-names>J</given-names><suffix>Jr</suffix></name><name><surname>Huang</surname><given-names>PH</given-names></name><name><surname>Tanos</surname><given-names>BE</given-names></name></person-group><year>2018</year><article-title>Primary cilia mediate diverse kinase inhibitor resistance mechanisms in cancer</article-title><source>Cell Rep</source><volume>23</volume><fpage>3042</fpage><lpage>3055</lpage><pub-id pub-id-type="doi">10.1016/j.celrep.2018.05.016</pub-id><pmc-comment>6016080 </pmc-comment>
<pub-id pub-id-type="pmid">29874589</pub-id></element-citation></ref><ref id="b16-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jonassen</surname><given-names>JA</given-names></name><name><surname>San Agustin</surname><given-names>J</given-names></name><name><surname>Follit</surname><given-names>JA</given-names></name><name><surname>Pazour</surname><given-names>GJ</given-names></name></person-group><year>2008</year><article-title>Deletion of IFT20 in the mouse kidney causes misorientation of the mitotic spindle and cystic kidney disease</article-title><source>J Cell Biol</source><volume>183</volume><fpage>377</fpage><lpage>384</lpage><pub-id pub-id-type="doi">10.1083/jcb.200808137</pub-id><pmc-comment>2575779 </pmc-comment>
<pub-id pub-id-type="pmid">18981227</pub-id></element-citation></ref><ref id="b17-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Jonassen</surname><given-names>JA</given-names></name><name><surname>SanAgustin</surname><given-names>J</given-names></name><name><surname>Baker</surname><given-names>SP</given-names></name><name><surname>Pazour</surname><given-names>GJ</given-names></name></person-group><year>2012</year><article-title>Disruption of IFT complex A causes cystic kidneys without mitotic spindle misorientation</article-title><source>J Am Soc Nephrol</source><volume>23</volume><fpage>641</fpage><lpage>651</lpage><pub-id pub-id-type="doi">10.1681/ASN.2011080829</pub-id><pmc-comment>3312512 </pmc-comment>
<pub-id pub-id-type="pmid">22282595</pub-id></element-citation></ref><ref id="b18-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kasahara</surname><given-names>K</given-names></name><name><surname>Kawakami</surname><given-names>Y</given-names></name><name><surname>Kiyono</surname><given-names>T</given-names></name><name><surname>Yonemura</surname><given-names>S</given-names></name><name><surname>Kawamura</surname><given-names>Y</given-names></name><name><surname>Era</surname><given-names>S</given-names></name><name><surname>Matsuzaki</surname><given-names>F</given-names></name><name><surname>Goshima</surname><given-names>N</given-names></name><name><surname>Inagaki</surname><given-names>M</given-names></name></person-group><year>2014</year><article-title>Ubiquitin-proteasome system controls ciliogenesis at the initial step of axoneme extension</article-title><source>Nat Commun</source><volume>5</volume><fpage>5081</fpage><pub-id pub-id-type="doi">10.1038/ncomms6081</pub-id><pmc-comment>4205846 </pmc-comment>
<pub-id pub-id-type="pmid">25270598</pub-id></element-citation></ref><ref id="b19-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kihara</surname><given-names>A</given-names></name><name><surname>Kabeya</surname><given-names>Y</given-names></name><name><surname>Ohsumi</surname><given-names>Y</given-names></name><name><surname>Yoshimori</surname><given-names>T</given-names></name></person-group><year>2001</year><article-title>Beclinphosphatidylinositol 3-kinase complex functions at the trans-Golgi network</article-title><source>EMBO Rep</source><volume>2</volume><fpage>330</fpage><lpage>335</lpage><pub-id pub-id-type="doi">10.1093/embo-reports/kve061</pub-id><pmc-comment>1083858 </pmc-comment>
<pub-id pub-id-type="pmid">11306555</pub-id></element-citation></ref><ref id="b20-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>ES</given-names></name><name><surname>Shin</surname><given-names>JH</given-names></name><name><surname>Park</surname><given-names>SJ</given-names></name><name><surname>Jo</surname><given-names>YK</given-names></name><name><surname>Kim</surname><given-names>JS</given-names></name><name><surname>Kang</surname><given-names>IH</given-names></name><name><surname>Nam</surname><given-names>JB</given-names></name><name><surname>Chung</surname><given-names>DY</given-names></name><name><surname>Cho</surname><given-names>Y</given-names></name><name><surname>Lee</surname><given-names>EH</given-names></name><name><surname>Chang</surname><given-names>JW</given-names></name><name><surname>Cho</surname><given-names>DH</given-names></name></person-group><year>2015a</year><article-title>Inhibition of autophagy suppresses sertraline-mediated primary ciliogenesis in retinal pigment epithelium cells</article-title><source>PLoS ONE</source><volume>10</volume><fpage>e0118190</fpage><pub-id pub-id-type="doi">10.1371/journal.pone.0118190</pub-id><pub-id pub-id-type="pmid">25671433</pub-id></element-citation></ref><ref id="b21-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kim</surname><given-names>J</given-names></name><name><surname>Jo</surname><given-names>H</given-names></name><name><surname>Hong</surname><given-names>H</given-names></name><name><surname>Kim</surname><given-names>MH</given-names></name><name><surname>Kim</surname><given-names>JM</given-names></name><name><surname>Lee</surname><given-names>JK</given-names></name><name><surname>Heo</surname><given-names>WD</given-names></name><name><surname>Kim</surname><given-names>J</given-names></name></person-group><year>2015b</year><article-title>Actin remodelling factors control ciliogenesis by regulating YAP/TAZ activity and vesicle trafficking</article-title><source>Nat Commun</source><volume>6</volume><fpage>6781</fpage><pub-id pub-id-type="doi">10.1038/ncomms7781</pub-id><pub-id pub-id-type="pmid">25849865</pub-id></element-citation></ref><ref id="b22-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Kobayashi</surname><given-names>T</given-names></name><name><surname>Itoh</surname><given-names>H</given-names></name></person-group><year>2017</year><article-title>Loss of a primary cilium in PDAC</article-title><source>Cell Cycle</source><volume>16</volume><fpage>817</fpage><lpage>818</lpage><pub-id pub-id-type="doi">10.1080/15384101.2017.1304738</pub-id><pmc-comment>5444347 </pmc-comment>
<pub-id pub-id-type="pmid">28319439</pub-id></element-citation></ref><ref id="b23-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lechtreck</surname><given-names>KF</given-names></name></person-group><year>2015</year><article-title>IFT-cargo interactions and protein transport in cilia</article-title><source>Trends Biochem Sci</source><volume>40</volume><fpage>765</fpage><lpage>778</lpage><pub-id pub-id-type="doi">10.1016/j.tibs.2015.09.003</pub-id><pmc-comment>4661101 </pmc-comment>
<pub-id pub-id-type="pmid">26498262</pub-id></element-citation></ref><ref id="b24-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>J</given-names></name><name><surname>Yi</surname><given-names>S</given-names></name><name><surname>Kang</surname><given-names>YE</given-names></name><name><surname>Chang</surname><given-names>JY</given-names></name><name><surname>Kim</surname><given-names>JT</given-names></name><name><surname>Sul</surname><given-names>HJ</given-names></name><name><surname>Kim</surname><given-names>JO</given-names></name><name><surname>Kim</surname><given-names>JM</given-names></name><name><surname>Kim</surname><given-names>J</given-names></name><name><surname>Porcelli</surname><given-names>AM</given-names></name><name><surname>Kim</surname><given-names>KS</given-names></name><name><surname>Shong</surname><given-names>M</given-names></name></person-group><year>2016</year><article-title>Defective ciliogenesis in thyroid hurthle cell tumors is associated with increased autophagy</article-title><source>Oncotarget</source><volume>7</volume><fpage>79117</fpage><lpage>79130</lpage><pub-id pub-id-type="doi">10.18632/oncotarget.12997</pub-id><pmc-comment>5346702 </pmc-comment>
<pub-id pub-id-type="pmid">27816963</pub-id></element-citation></ref><ref id="b25-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Liu</surname><given-names>ZQ</given-names></name><name><surname>Lee</surname><given-names>JN</given-names></name><name><surname>Son</surname><given-names>M</given-names></name><name><surname>Lim</surname><given-names>JY</given-names></name><name><surname>Dutta</surname><given-names>RK</given-names></name><name><surname>Maharjan</surname><given-names>Y</given-names></name><name><surname>Kwak</surname><given-names>S</given-names></name><name><surname>Oh</surname><given-names>GT</given-names></name><name><surname>Byun</surname><given-names>K</given-names></name><name><surname>Choe</surname><given-names>SK</given-names></name><name><surname>Park</surname><given-names>R</given-names></name></person-group><year>2018</year><article-title>Ciliogenesis is reciprocally regulated by PPARA and NR1H4/FXR through controlling autophagy in vitro and in vivo</article-title><source>Autophagy</source><volume>14</volume><fpage>1011</fpage><lpage>1027</lpage><pmc-comment>6103415 </pmc-comment>
<pub-id pub-id-type="pmid">29771182</pub-id></element-citation></ref><ref id="b26-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Malicki</surname><given-names>JJ</given-names></name><name><surname>Johnson</surname><given-names>CA</given-names></name></person-group><year>2017</year><article-title>The cilium: cellular antenna and central processing unit</article-title><source>Trends Cell Biol</source><volume>27</volume><fpage>126</fpage><lpage>140</lpage><pub-id pub-id-type="doi">10.1016/j.tcb.2016.08.002</pub-id><pmc-comment>5278183 </pmc-comment>
<pub-id pub-id-type="pmid">27634431</pub-id></element-citation></ref><ref id="b27-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mauthe</surname><given-names>M</given-names></name><name><surname>Orhon</surname><given-names>I</given-names></name><name><surname>Rocchi</surname><given-names>C</given-names></name><name><surname>Zhou</surname><given-names>X</given-names></name><name><surname>Luhr</surname><given-names>M</given-names></name><name><surname>Hijlkema</surname><given-names>KJ</given-names></name><name><surname>Coppes</surname><given-names>RP</given-names></name><name><surname>Engedal</surname><given-names>N</given-names></name><name><surname>Mari</surname><given-names>M</given-names></name><name><surname>Reggiori</surname><given-names>F</given-names></name></person-group><year>2018</year><article-title>Chloroquine inhibits autophagic flux by decreasing autophagosomelysosome fusion</article-title><source>Autophagy</source><volume>14</volume><fpage>1435</fpage><lpage>1455</lpage><pub-id pub-id-type="doi">10.1080/15548627.2018.1474314</pub-id><pub-id pub-id-type="pmid">29940786</pub-id></element-citation></ref><ref id="b28-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Menzl</surname><given-names>I</given-names></name><name><surname>Lebeau</surname><given-names>L</given-names></name><name><surname>Pandey</surname><given-names>R</given-names></name><name><surname>Hassounah</surname><given-names>NB</given-names></name><name><surname>Li</surname><given-names>FW</given-names></name><name><surname>Nagle</surname><given-names>R</given-names></name><name><surname>Weihs</surname><given-names>K</given-names></name><name><surname>McDermott</surname><given-names>KM</given-names></name></person-group><year>2014</year><article-title>Loss of primary cilia occurs early in breast cancer development</article-title><source>Cilia</source><volume>3</volume><fpage>7</fpage><pub-id pub-id-type="doi">10.1186/2046-2530-3-7</pub-id><pmc-comment>4076761 </pmc-comment>
<pub-id pub-id-type="pmid">24987519</pub-id></element-citation></ref><ref id="b29-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Mizushima</surname><given-names>N</given-names></name><name><surname>Yoshimori</surname><given-names>T</given-names></name><name><surname>Ohsumi</surname><given-names>Y</given-names></name></person-group><year>2011</year><article-title>The role of Atg proteins in autophagosome formation</article-title><source>Annu Rev Cell Dev Biol</source><volume>27</volume><fpage>107</fpage><lpage>132</lpage><pub-id pub-id-type="doi">10.1146/annurev-cellbio-092910-154005</pub-id><pub-id pub-id-type="pmid">21801009</pub-id></element-citation></ref><ref id="b30-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Moon</surname><given-names>H</given-names></name><name><surname>Song</surname><given-names>J</given-names></name><name><surname>Shin</surname><given-names>JO</given-names></name><name><surname>Lee</surname><given-names>H</given-names></name><name><surname>Kim</surname><given-names>HK</given-names></name><name><surname>Eggenschwiller</surname><given-names>JT</given-names></name><name><surname>Bok</surname><given-names>J</given-names></name><name><surname>Ko</surname><given-names>HW</given-names></name></person-group><year>2014</year><article-title>Intestinal cell kinase, a protein associated with endocrine-cerebro-osteodysplasia syndrome, is a key regulator of cilia length and Hedgehog signaling</article-title><source>Proc Natl Acad Sci USA</source><volume>111</volume><fpage>8541</fpage><lpage>8546</lpage><pub-id pub-id-type="doi">10.1073/pnas.1323161111</pub-id><pmc-comment>4060650 </pmc-comment>
<pub-id pub-id-type="pmid">24853502</pub-id></element-citation></ref><ref id="b31-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Nakatogawa</surname><given-names>H</given-names></name><name><surname>Ichimura</surname><given-names>Y</given-names></name><name><surname>Ohsumi</surname><given-names>Y</given-names></name></person-group><year>2007</year><article-title>Atg8, a ubiquitin-like protein required for autophagosome formation, mediates membrane tethering and hemifusion</article-title><source>Cell</source><volume>130</volume><fpage>165</fpage><lpage>178</lpage><pub-id pub-id-type="doi">10.1016/j.cell.2007.05.021</pub-id><pub-id pub-id-type="pmid">17632063</pub-id></element-citation></ref><ref id="b32-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Nobutani</surname><given-names>K</given-names></name><name><surname>Shimono</surname><given-names>Y</given-names></name><name><surname>Yoshida</surname><given-names>M</given-names></name><name><surname>Mizutani</surname><given-names>K</given-names></name><name><surname>Minami</surname><given-names>A</given-names></name><name><surname>Kono</surname><given-names>S</given-names></name><name><surname>Mukohara</surname><given-names>T</given-names></name><name><surname>Yamasaki</surname><given-names>T</given-names></name><name><surname>Itoh</surname><given-names>T</given-names></name><name><surname>Takao</surname><given-names>S</given-names></name><name><surname>Minami</surname><given-names>H</given-names></name><name><surname>Azuma</surname><given-names>T</given-names></name><name><surname>Takai</surname><given-names>Y</given-names></name></person-group><year>2014</year><article-title>Absence of primary cilia in cell cycle-arrested human breast cancer cells</article-title><source>Genes Cells</source><volume>19</volume><fpage>141</fpage><lpage>152</lpage><pub-id pub-id-type="doi">10.1111/gtc.12122</pub-id><pub-id pub-id-type="pmid">24330390</pub-id></element-citation></ref><ref id="b33-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Okada</surname><given-names>Y</given-names></name><name><surname>Nonaka</surname><given-names>S</given-names></name><name><surname>Tanaka</surname><given-names>Y</given-names></name><name><surname>Saijoh</surname><given-names>Y</given-names></name><name><surname>Hamada</surname><given-names>H</given-names></name><name><surname>Hirokawa</surname><given-names>N</given-names></name></person-group><year>1999</year><article-title>Abnormal nodal flow precedes situs inversus in iv and inv mice</article-title><source>Mol. Cell</source><volume>4</volume><fpage>459</fpage><lpage>468</lpage><pub-id pub-id-type="doi">10.1016/S1097-2765(00)80197-5</pub-id><pub-id pub-id-type="pmid">10549278</pub-id></element-citation></ref><ref id="b34-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pampliega</surname><given-names>O</given-names></name><name><surname>Cuervo</surname><given-names>AM</given-names></name></person-group><year>2016</year><article-title>Autophagy and primary cilia: dual interplay</article-title><source>Curr Opin Cell Biol</source><volume>39</volume><fpage>1</fpage><lpage>7</lpage><pub-id pub-id-type="doi">10.1016/j.ceb.2016.01.008</pub-id><pmc-comment>4733852 </pmc-comment>
<pub-id pub-id-type="pmid">26826446</pub-id></element-citation></ref><ref id="b35-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pampliega</surname><given-names>O</given-names></name><name><surname>Orhon</surname><given-names>I</given-names></name><name><surname>Patel</surname><given-names>B</given-names></name><name><surname>Sridhar</surname><given-names>S</given-names></name><name><surname>Diaz-Carretero</surname><given-names>A</given-names></name><name><surname>Beau</surname><given-names>I</given-names></name><name><surname>Codogno</surname><given-names>P</given-names></name><name><surname>Satir</surname><given-names>BH</given-names></name><name><surname>Satir</surname><given-names>P</given-names></name><name><surname>Cuervo</surname><given-names>AM</given-names></name></person-group><year>2013</year><article-title>Functional interaction between autophagy and ciliogenesis</article-title><source>Nature</source><volume>502</volume><fpage>194</fpage><lpage>200</lpage><pub-id pub-id-type="doi">10.1038/nature12639</pub-id><pmc-comment>3896125 </pmc-comment>
<pub-id pub-id-type="pmid">24089209</pub-id></element-citation></ref><ref id="b36-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Plotnikova</surname><given-names>OV</given-names></name><name><surname>Nikonova</surname><given-names>AS</given-names></name><name><surname>Loskutov</surname><given-names>YV</given-names></name><name><surname>Kozyulina</surname><given-names>PY</given-names></name><name><surname>Pugacheva</surname><given-names>EN</given-names></name><name><surname>Golemis</surname><given-names>EA</given-names></name></person-group><year>2012</year><article-title>Calmodulin activation of Aurora-A kinase (AURKA) is required during ciliary disassembly and in mitosis</article-title><source>Mol. Biol. Cell</source><volume>23</volume><fpage>2658</fpage><lpage>2670</lpage><pub-id pub-id-type="doi">10.1091/mbc.e11-12-1056</pub-id><pmc-comment>3395655 </pmc-comment>
<pub-id pub-id-type="pmid">22621899</pub-id></element-citation></ref><ref id="b37-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Plotnikova</surname><given-names>OV</given-names></name><name><surname>Pugacheva</surname><given-names>EN</given-names></name><name><surname>Golemis</surname><given-names>EA</given-names></name></person-group><year>2009</year><article-title>Primary cilia and the cell cycle</article-title><source>Methods Cell Biol</source><volume>94</volume><fpage>137</fpage><lpage>160</lpage><pub-id pub-id-type="doi">10.1016/S0091-679X(08)94007-3</pub-id><pmc-comment>2852269 </pmc-comment>
<pub-id pub-id-type="pmid">20362089</pub-id></element-citation></ref><ref id="b38-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Pugacheva</surname><given-names>EN</given-names></name><name><surname>Jablonski</surname><given-names>SA</given-names></name><name><surname>Hartman</surname><given-names>TR</given-names></name><name><surname>Henske</surname><given-names>EP</given-names></name><name><surname>Golemis</surname><given-names>EA</given-names></name></person-group><year>2007</year><article-title>HEF1-dependent Aurora A activation induces disassembly of the primary cilium</article-title><source>Cell</source><volume>129</volume><fpage>1351</fpage><lpage>1363</lpage><pub-id pub-id-type="doi">10.1016/j.cell.2007.04.035</pub-id><pmc-comment>2504417 </pmc-comment>
<pub-id pub-id-type="pmid">17604723</pub-id></element-citation></ref><ref id="b39-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Ritter</surname><given-names>A</given-names></name><name><surname>Friemel</surname><given-names>A</given-names></name><name><surname>Kreis</surname><given-names>NN</given-names></name><name><surname>Hoock</surname><given-names>SC</given-names></name><name><surname>Roth</surname><given-names>S</given-names></name><name><surname>Kielland-Kaisen</surname><given-names>U</given-names></name><name><surname>Bruggmann</surname><given-names>D</given-names></name><name><surname>Solbach</surname><given-names>C</given-names></name><name><surname>Louwen</surname><given-names>F</given-names></name><name><surname>Yuan</surname><given-names>J</given-names></name></person-group><year>2018</year><article-title>Primary cilia are dysfunctional in obese adipose-derived mesenchymal stem cells</article-title><source>Stem Cell Reports</source><volume>10</volume><fpage>583</fpage><lpage>599</lpage><pub-id pub-id-type="doi">10.1016/j.stemcr.2017.12.022</pub-id><pmc-comment>5830986 </pmc-comment>
<pub-id pub-id-type="pmid">29396182</pub-id></element-citation></ref><ref id="b40-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Seeley</surname><given-names>ES</given-names></name><name><surname>Carriere</surname><given-names>C</given-names></name><name><surname>Goetze</surname><given-names>T</given-names></name><name><surname>Longnecker</surname><given-names>DS</given-names></name><name><surname>Korc</surname><given-names>M</given-names></name></person-group><year>2009a</year><article-title>Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia</article-title><source>Cancer Res</source><volume>69</volume><fpage>422</fpage><lpage>430</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-08-1290</pub-id><pub-id pub-id-type="pmid">19147554</pub-id></element-citation></ref><ref id="b41-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Seeley</surname><given-names>ES</given-names></name><name><surname>Carriere</surname><given-names>C</given-names></name><name><surname>Goetze</surname><given-names>T</given-names></name><name><surname>Longnecker</surname><given-names>DS</given-names></name><name><surname>Korc</surname><given-names>M</given-names></name></person-group><year>2009b</year><article-title>Pancreatic cancer and precursor pancreatic intraepithelial neoplasia lesions are devoid of primary cilia</article-title><source>Cancer Res</source><volume>69</volume><fpage>422</fpage><lpage>430</lpage><pub-id pub-id-type="doi">10.1158/0008-5472.CAN-08-1290</pub-id><pub-id pub-id-type="pmid">19147554</pub-id></element-citation></ref><ref id="b42-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Servattalab</surname><given-names>S</given-names></name><name><surname>Yildiz</surname><given-names>O</given-names></name><name><surname>Khanna</surname><given-names>H</given-names></name></person-group><year>2012</year><article-title>Tackling primary cilia dysfunction in photoreceptor degenerative diseases of the eye</article-title><source>Int. J. Ophthalmic. Pathol</source><volume>1</volume><fpage>e101</fpage><pmc-comment>3894363 </pmc-comment>
<pub-id pub-id-type="pmid">24455751</pub-id></element-citation></ref><ref id="b43-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shin</surname><given-names>JH</given-names></name><name><surname>Bae</surname><given-names>DJ</given-names></name><name><surname>Kim</surname><given-names>ES</given-names></name><name><surname>Kim</surname><given-names>HB</given-names></name><name><surname>Park</surname><given-names>SJ</given-names></name><name><surname>Jo</surname><given-names>YK</given-names></name><name><surname>Jo</surname><given-names>DS</given-names></name><name><surname>Jo</surname><given-names>DG</given-names></name><name><surname>Kim</surname><given-names>SY</given-names></name><name><surname>Cho</surname><given-names>DH</given-names></name></person-group><year>2015a</year><article-title>Autophagy regulates formation of primary cilia in mefloquine-treated cells</article-title><source>Biomol Ther (Seoul)</source><volume>23</volume><fpage>327</fpage><lpage>232</lpage><pub-id pub-id-type="doi">10.4062/biomolther.2015.025</pub-id><pub-id pub-id-type="pmid">26157548</pub-id></element-citation></ref><ref id="b44-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Shin</surname><given-names>JH</given-names></name><name><surname>Kim</surname><given-names>PS</given-names></name><name><surname>Kim</surname><given-names>ES</given-names></name><name><surname>Park</surname><given-names>SJ</given-names></name><name><surname>Jo</surname><given-names>YK</given-names></name><name><surname>Hwang</surname><given-names>JJ</given-names></name><name><surname>Park</surname><given-names>TJ</given-names></name><name><surname>Chang</surname><given-names>JW</given-names></name><name><surname>Seo</surname><given-names>JH</given-names></name><name><surname>Cho</surname><given-names>DH</given-names></name></person-group><year>2015b</year><article-title>BIX-01294-induced autophagy regulates elongation of primary cilia</article-title><source>Biochem Biophys Res Commun</source><volume>460</volume><fpage>428</fpage><lpage>433</lpage><pub-id pub-id-type="doi">10.1016/j.bbrc.2015.03.050</pub-id><pub-id pub-id-type="pmid">25796328</pub-id></element-citation></ref><ref id="b45-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Song</surname><given-names>DK</given-names></name><name><surname>Choi</surname><given-names>JH</given-names></name><name><surname>Kim</surname><given-names>MS</given-names></name></person-group><year>2018</year><article-title>Primary cilia as a signaling platform for control of energy metabolism</article-title><source>Diabetes Metab J</source><volume>42</volume><fpage>117</fpage><lpage>127</lpage><pub-id pub-id-type="doi">10.4093/dmj.2018.42.2.117</pub-id><pmc-comment>5911514 </pmc-comment>
<pub-id pub-id-type="pmid">29676541</pub-id></element-citation></ref><ref id="b46-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Stanley</surname><given-names>RE</given-names></name><name><surname>Ragusa</surname><given-names>MJ</given-names></name><name><surname>Hurley</surname><given-names>JH</given-names></name></person-group><year>2014</year><article-title>The beginning of the end: how scaffolds nucleate autophagosome biogenesis</article-title><source>Trends Cell Biol</source><volume>24</volume><fpage>73</fpage><lpage>81</lpage><pub-id pub-id-type="doi">10.1016/j.tcb.2013.07.008</pub-id><pub-id pub-id-type="pmid">23999079</pub-id></element-citation></ref><ref id="b47-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Struchtrup</surname><given-names>A</given-names></name><name><surname>Wiegering</surname><given-names>A</given-names></name><name><surname>Stork</surname><given-names>B</given-names></name><name><surname>Ruther</surname><given-names>U</given-names></name><name><surname>Gerhardt</surname><given-names>C</given-names></name></person-group><year>2018</year><article-title>The ciliary protein RPGRIP1L governs autophagy independently of its proteasome-regulating function at the ciliary base in mouse embryonic fibroblasts</article-title><source>Autophagy</source><volume>14</volume><fpage>567</fpage><lpage>583</lpage><pub-id pub-id-type="doi">10.1080/15548627.2018.1429874</pub-id><pmc-comment>5959336 </pmc-comment>
<pub-id pub-id-type="pmid">29372668</pub-id></element-citation></ref><ref id="b48-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Takahashi</surname><given-names>K</given-names></name><name><surname>Nagai</surname><given-names>T</given-names></name><name><surname>Chiba</surname><given-names>S</given-names></name><name><surname>Nakayama</surname><given-names>K</given-names></name><name><surname>Mizuno</surname><given-names>K</given-names></name></person-group><year>2018</year><article-title>Glucose deprivation induces primary cilium formation through mTORC1 inactivation</article-title><source>J. Cell Sci</source><volume>131</volume><fpage>jcs208769</fpage><pub-id pub-id-type="doi">10.1242/jcs.208769</pub-id><pub-id pub-id-type="pmid">29180513</pub-id></element-citation></ref><ref id="b49-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tang</surname><given-names>Z</given-names></name><name><surname>Lin</surname><given-names>MG</given-names></name><name><surname>Stowe</surname><given-names>TR</given-names></name><name><surname>Chen</surname><given-names>S</given-names></name><name><surname>Zhu</surname><given-names>M</given-names></name><name><surname>Stearns</surname><given-names>T</given-names></name><name><surname>Franco</surname><given-names>B</given-names></name><name><surname>Zhong</surname><given-names>Q</given-names></name></person-group><year>2013</year><article-title>Autophagy promotes primary ciliogenesis by removing OFD1 from centriolar satellites</article-title><source>Nature</source><volume>502</volume><fpage>254</fpage><lpage>257</lpage><pub-id pub-id-type="doi">10.1038/nature12606</pub-id><pmc-comment>4075283 </pmc-comment>
<pub-id pub-id-type="pmid">24089205</pub-id></element-citation></ref><ref id="b50-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Taschner</surname><given-names>M</given-names></name><name><surname>Bhogaraju</surname><given-names>S</given-names></name><name><surname>Lorentzen</surname><given-names>E</given-names></name></person-group><year>2012</year><article-title>Architecture and function of IFT complex proteins in ciliogenesis</article-title><source>Differentiation</source><volume>83</volume><fpage>S12</fpage><lpage>S22</lpage><pub-id pub-id-type="doi">10.1016/j.diff.2011.11.001</pub-id><pub-id pub-id-type="pmid">22118932</pub-id></element-citation></ref><ref id="b51-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Taylor</surname><given-names>SP</given-names></name><name><surname>Dantas</surname><given-names>TJ</given-names></name><name><surname>Duran</surname><given-names>I</given-names></name><name><surname>Wu</surname><given-names>S</given-names></name><name><surname>Lachman</surname><given-names>RS</given-names></name><collab>University of Washington Center for Mendelian Genomics Consortium</collab><name><surname>Nelson</surname><given-names>SF</given-names></name><name><surname>Cohn</surname><given-names>DH</given-names></name><name><surname>Vallee</surname><given-names>RB</given-names></name><name><surname>Krakow</surname><given-names>D</given-names></name></person-group><year>2015</year><article-title>Mutations in DYNC2LI1 disrupt cilia function and cause short rib polydactyly syndrome</article-title><source>Nat Commun</source><volume>6</volume><fpage>7092</fpage><pub-id pub-id-type="doi">10.1038/ncomms8092</pub-id><pmc-comment>4470332 </pmc-comment>
<pub-id pub-id-type="pmid">26077881</pub-id></element-citation></ref><ref id="b52-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Tong</surname><given-names>Y</given-names></name><name><surname>Park</surname><given-names>SH</given-names></name><name><surname>Wu</surname><given-names>D</given-names></name><name><surname>Xu</surname><given-names>W</given-names></name><name><surname>Guillot</surname><given-names>SJ</given-names></name><name><surname>Jin</surname><given-names>L</given-names></name><name><surname>Li</surname><given-names>X</given-names></name><name><surname>Wang</surname><given-names>Y</given-names></name><name><surname>Lin</surname><given-names>CS</given-names></name><name><surname>Fu</surname><given-names>Z</given-names></name></person-group><year>2017</year><article-title>An essential role of intestinal cell kinase in lung development is linked to the perinatal lethality of human ECO syndrome</article-title><source>FEBS Lett</source><volume>591</volume><fpage>1247</fpage><lpage>1257</lpage><pub-id pub-id-type="doi">10.1002/1873-3468.12644</pub-id><pmc-comment>5466854 </pmc-comment>
<pub-id pub-id-type="pmid">28380258</pub-id></element-citation></ref><ref id="b53-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Volta</surname><given-names>F</given-names></name><name><surname>Gerdes</surname><given-names>JM</given-names></name></person-group><year>2017</year><article-title>The role of primary cilia in obesity and diabetes</article-title><source>Ann N Y Acad Sci</source><volume>1391</volume><fpage>71</fpage><lpage>84</lpage><pub-id pub-id-type="doi">10.1111/nyas.13216</pub-id><pub-id pub-id-type="pmid">27706820</pub-id></element-citation></ref><ref id="b54-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>S</given-names></name><name><surname>Livingston</surname><given-names>MJ</given-names></name><name><surname>Su</surname><given-names>Y</given-names></name><name><surname>Dong</surname><given-names>Z</given-names></name></person-group><year>2015</year><article-title>Reciprocal regulation of cilia and autophagy via the MTOR and proteasome pathways</article-title><source>Autophagy</source><volume>11</volume><fpage>607</fpage><lpage>616</lpage><pub-id pub-id-type="doi">10.1080/15548627.2015.1023983</pub-id><pmc-comment>4502771 </pmc-comment>
<pub-id pub-id-type="pmid">25906314</pub-id></element-citation></ref><ref id="b55-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wang</surname><given-names>ZL</given-names></name><name><surname>Deng</surname><given-names>Q</given-names></name><name><surname>Chong</surname><given-names>T</given-names></name><name><surname>Wang</surname><given-names>ZM</given-names></name></person-group><year>2018</year><article-title>Autophagy suppresses the proliferation of renal carcinoma cell</article-title><source>Eur Rev Med Pharmacol Sci</source><volume>22</volume><fpage>343</fpage><lpage>350</lpage><pub-id pub-id-type="pmid">29424891</pub-id></element-citation></ref><ref id="b56-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wheway</surname><given-names>G</given-names></name><name><surname>Parry</surname><given-names>DA</given-names></name><name><surname>Johnson</surname><given-names>CA</given-names></name></person-group><year>2014</year><article-title>The role of primary cilia in the development and disease of the retina</article-title><source>Organogenesis</source><volume>10</volume><fpage>69</fpage><lpage>85</lpage><pub-id pub-id-type="doi">10.4161/org.26710</pub-id><pmc-comment>4049897 </pmc-comment>
<pub-id pub-id-type="pmid">24162842</pub-id></element-citation></ref><ref id="b57-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>White</surname><given-names>E</given-names></name></person-group><year>2015</year><article-title>The role for autophagy in cancer</article-title><source>J Clin Invest</source><volume>125</volume><fpage>42</fpage><lpage>46</lpage><pub-id pub-id-type="doi">10.1172/JCI73941</pub-id><pmc-comment>4382247 </pmc-comment>
<pub-id pub-id-type="pmid">25654549</pub-id></element-citation></ref><ref id="b58-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Wiegering</surname><given-names>A</given-names></name><name><surname>Ruther</surname><given-names>U</given-names></name><name><surname>Gerhardt</surname><given-names>C</given-names></name></person-group><year>2019</year><article-title>The role of primary cilia in the crosstalk between the ubiquitin-proteasome system and autophagy</article-title><source>Cells</source><volume>8</volume><fpage>241</fpage><pub-id pub-id-type="doi">10.3390/cells8030241</pub-id></element-citation></ref><ref id="b59-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xiao</surname><given-names>ZS</given-names></name><name><surname>Quarles</surname><given-names>LD</given-names></name></person-group><year>2010</year><article-title>Role of the polycytin-primary cilia complex in bone development and mechanosensing</article-title><source>Ann N Y Acad Sci</source><volume>1192</volume><fpage>410</fpage><lpage>421</lpage><pub-id pub-id-type="doi">10.1111/j.1749-6632.2009.05239.x</pub-id><pmc-comment>2924156 </pmc-comment>
<pub-id pub-id-type="pmid">20392267</pub-id></element-citation></ref><ref id="b60-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>Q</given-names></name><name><surname>Liu</surname><given-names>W</given-names></name><name><surname>Liu</surname><given-names>X</given-names></name><name><surname>Liu</surname><given-names>W</given-names></name><name><surname>Wang</surname><given-names>H</given-names></name><name><surname>Yao</surname><given-names>G</given-names></name><name><surname>Zang</surname><given-names>L</given-names></name><name><surname>Hayashi</surname><given-names>T</given-names></name><name><surname>Tashiro</surname><given-names>S</given-names></name><name><surname>Onodera</surname><given-names>S</given-names></name><name><surname>Ikejima</surname><given-names>T</given-names></name></person-group><year>2016</year><article-title>Silibinin negatively contributes to primary cilia length via autophagy regulated by histone deacetylase 6 in confluent mouse embryo fibroblast 3T3-L1 cells</article-title><source>Mol Cell Biochem</source><volume>420</volume><fpage>53</fpage><lpage>63</lpage><pub-id pub-id-type="doi">10.1007/s11010-016-2766-2</pub-id><pub-id pub-id-type="pmid">27435857</pub-id></element-citation></ref><ref id="b61-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Xu</surname><given-names>Q</given-names></name><name><surname>Liu</surname><given-names>W</given-names></name><name><surname>Liu</surname><given-names>X</given-names></name><name><surname>Otkur</surname><given-names>W</given-names></name><name><surname>Hayashi</surname><given-names>T</given-names></name><name><surname>Yamato</surname><given-names>M</given-names></name><name><surname>Fujisaki</surname><given-names>H</given-names></name><name><surname>Hattori</surname><given-names>S</given-names></name><name><surname>Tashiro</surname><given-names>SI</given-names></name><name><surname>Ikejima</surname><given-names>T</given-names></name></person-group><year>2018</year><article-title>Type I collagen promotes primary cilia growth through down-regulating HDAC6-mediated autophagy in confluent mouse embryo fibroblast 3T3-L1 cells</article-title><source>J Biosci Bioeng</source><volume>125</volume><fpage>8</fpage><lpage>14</lpage><pub-id pub-id-type="doi">10.1016/j.jbiosc.2017.07.012</pub-id><pub-id pub-id-type="pmid">28811097</pub-id></element-citation></ref><ref id="b62-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yang</surname><given-names>SH</given-names></name><name><surname>Wang</surname><given-names>XX</given-names></name><name><surname>Contino</surname><given-names>G</given-names></name><name><surname>Liesa</surname><given-names>M</given-names></name><name><surname>Sahin</surname><given-names>E</given-names></name><name><surname>Ying</surname><given-names>HQ</given-names></name><name><surname>Bause</surname><given-names>A</given-names></name><name><surname>Li</surname><given-names>YH</given-names></name><name><surname>Stommel</surname><given-names>JM</given-names></name><name><surname>Dell’Antonio</surname><given-names>G</given-names></name><name><surname>Mautner</surname><given-names>J</given-names></name><name><surname>Tonon</surname><given-names>G</given-names></name><name><surname>Haigis</surname><given-names>M</given-names></name><name><surname>Shirihai</surname><given-names>OS</given-names></name><name><surname>Doglioni</surname><given-names>C</given-names></name><name><surname>Bardeesy</surname><given-names>N</given-names></name><name><surname>Kimmelman</surname><given-names>AC</given-names></name></person-group><year>2011</year><article-title>Pancreatic cancers require autophagy for tumor growth</article-title><source>Genes Dev</source><volume>25</volume><fpage>717</fpage><lpage>729</lpage><pub-id pub-id-type="doi">10.1101/gad.2016111</pub-id><pmc-comment>3070934 </pmc-comment>
<pub-id pub-id-type="pmid">21406549</pub-id></element-citation></ref><ref id="b63-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Youn</surname><given-names>YH</given-names></name><name><surname>Han</surname><given-names>YG</given-names></name></person-group><year>2018</year><article-title>Primary cilia in brain development and diseases</article-title><source>Am J Pathol</source><volume>188</volume><fpage>11</fpage><lpage>22</lpage><pub-id pub-id-type="doi">10.1016/j.ajpath.2017.08.031</pub-id><pmc-comment>5745523 </pmc-comment>
<pub-id pub-id-type="pmid">29030052</pub-id></element-citation></ref><ref id="b64-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Yuan</surname><given-names>K</given-names></name><name><surname>Frolova</surname><given-names>N</given-names></name><name><surname>Xie</surname><given-names>Y</given-names></name><name><surname>Wang</surname><given-names>D</given-names></name><name><surname>Cook</surname><given-names>L</given-names></name><name><surname>Kwon</surname><given-names>YJ</given-names></name><name><surname>Steg</surname><given-names>AD</given-names></name><name><surname>Serra</surname><given-names>R</given-names></name><name><surname>Frost</surname><given-names>AR</given-names></name></person-group><year>2010</year><article-title>Primary cilia are decreased in breast cancer: analysis of a collection of human breast cancer cell lines and tissues</article-title><source>J Histochem Cytochem</source><volume>58</volume><fpage>857</fpage><lpage>870</lpage><pub-id pub-id-type="doi">10.1369/jhc.2010.955856</pub-id><pmc-comment>2942739 </pmc-comment>
<pub-id pub-id-type="pmid">20530462</pub-id></element-citation></ref><ref id="b65-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhao</surname><given-names>YG</given-names></name><name><surname>Zhang</surname><given-names>H</given-names></name></person-group><year>2019</year><article-title>Autophagosome maturation: an epic journey from the ER to lysosomes</article-title><source>J Cell Biol</source><volume>218</volume><fpage>757</fpage><lpage>770</lpage><pub-id pub-id-type="doi">10.1083/jcb.201810099</pub-id><pub-id pub-id-type="pmid">30578282</pub-id></element-citation></ref><ref id="b66-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zhi</surname><given-names>X</given-names></name><name><surname>Zhong</surname><given-names>Q</given-names></name></person-group><year>2015</year><article-title>Autophagy in cancer</article-title><source>F1000Prime Rep</source><volume>7</volume><fpage>18</fpage><pub-id pub-id-type="doi">10.12703/P7-18</pub-id><pmc-comment>4338832 </pmc-comment>
<pub-id pub-id-type="pmid">25750736</pub-id></element-citation></ref><ref id="b67-bt-27-337"><element-citation publication-type="journal"><person-group person-group-type="author"><name><surname>Zingg</surname><given-names>D</given-names></name><name><surname>Debbache</surname><given-names>J</given-names></name><name><surname>Pena-Hernandez</surname><given-names>R</given-names></name><name><surname>Antunes</surname><given-names>AT</given-names></name><name><surname>Schaefer</surname><given-names>SM</given-names></name><name><surname>Cheng</surname><given-names>PF</given-names></name><name><surname>Zimmerli</surname><given-names>D</given-names></name><name><surname>Haeusel</surname><given-names>J</given-names></name><name><surname>Calcada</surname><given-names>RR</given-names></name><name><surname>Tuncer</surname><given-names>E</given-names></name><name><surname>Zhang</surname><given-names>Y</given-names></name><name><surname>Bossart</surname><given-names>R</given-names></name><name><surname>Wong</surname><given-names>KK</given-names></name><name><surname>Basler</surname><given-names>K</given-names></name><name><surname>Dummer</surname><given-names>R</given-names></name><name><surname>Santoro</surname><given-names>R</given-names></name><name><surname>Levesque</surname><given-names>MP</given-names></name><name><surname>Sommer</surname><given-names>L</given-names></name></person-group><year>2018</year><article-title>EZH2-mediated primary cilium deconstruction drives metastatic melanoma formation</article-title><source>Cancer Cell</source><volume>34</volume><fpage>69</fpage><lpage>84.e14</lpage><pub-id pub-id-type="doi">10.1016/j.ccell.2018.06.001</pub-id><pub-id pub-id-type="pmid">30008323</pub-id></element-citation></ref></ref-list></back><floats-group><fig id="f1-bt-27-337" orientation="portrait" position="float"><label>Fig. 1.</label><caption><p>Controversial interplay between primary cilia and autophagy and effect of autophagy inhibitors in cancer cells. (A) Proposed model for the positive correlation between primary cilia and autophagy involving OFD1 protein in normal cells (B) Pancreatic ductal adenocarcinoma (PDAC) cells with increased autophagy activity despite absence of primary cilia. In this cancer cell, the autophagy inhibitor, chloroquine (CQ), shows therapeutic effect. (C) XTC.UC1 cells derived from thyroid Hürthle cell carcinoma with increased autophagy activity despite decreased frequency of ciliated cells. In this cancer cell, the autophagy inhibitor, 3-MA, increases frequency of ciliated XTC.UC1 cells via accumulation of ciliary proteins, such as IFT88 and ARL13B.</p></caption><graphic xlink:href="bt-27-337f1"></graphic></fig></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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