Autophagic homeostasis is required for the pluripotency of cancer stem cells.
Identifieur interne : 000923 ( Main/Corpus ); précédent : 000922; suivant : 000924Autophagic homeostasis is required for the pluripotency of cancer stem cells.
Auteurs : Tanveer Sharif ; Emma Martell ; Cathleen Dai ; Barry E. Kennedy ; Patrick Murphy ; Derek R. Clements ; Youra Kim ; Patrick W K. Lee ; Shashi A. GujarSource :
- Autophagy [ 1554-8635 ] ; 2017.
English descriptors
- KwdEn :
- Animals (MeSH), Autophagy (drug effects), Beclin-1 (metabolism), Cell Differentiation (drug effects), Cell Proliferation (drug effects), Cell Survival (drug effects), Cellular Senescence (drug effects), Cytokines (antagonists & inhibitors), Cytokines (metabolism), Doxorubicin (pharmacology), Homeostasis (drug effects), Mice (MeSH), Models, Biological (MeSH), Neoplastic Stem Cells (drug effects), Neoplastic Stem Cells (enzymology), Neoplastic Stem Cells (pathology), Nicotinamide Phosphoribosyltransferase (antagonists & inhibitors), Nicotinamide Phosphoribosyltransferase (metabolism), Octamer Transcription Factor-3 (metabolism), PTEN Phosphohydrolase (metabolism), Phosphorylation (drug effects), Pluripotent Stem Cells (drug effects), Pluripotent Stem Cells (pathology), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Cytokines, Nicotinamide Phosphoribosyltransferase.
- chemical , metabolism : Beclin-1, Cytokines, Nicotinamide Phosphoribosyltransferase, Octamer Transcription Factor-3, PTEN Phosphohydrolase, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- drug effects : Autophagy, Cell Differentiation, Cell Proliferation, Cell Survival, Cellular Senescence, Homeostasis, Neoplastic Stem Cells, Phosphorylation, Pluripotent Stem Cells.
- enzymology : Neoplastic Stem Cells.
- pathology : Neoplastic Stem Cells, Pluripotent Stem Cells.
- chemical , pharmacology : Doxorubicin, Sirolimus.
- Animals, Mice, Models, Biological, Signal Transduction.
Abstract
Pluripotency is an important feature of cancer stem cells (CSCs) that contributes to self-renewal and chemoresistance. The maintenance of pluripotency of CSCs under various pathophysiological conditions requires a complex interaction between various cellular pathways including those involved in homeostasis and energy metabolism. However, the exact mechanisms that maintain the CSC pluripotency remain poorly understood. In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD+ synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1). First, our data show that the pharmacological inhibition and knockdown (KD) of NAMPT or the KD of POU5F1 in human CSCs significantly decreased the expression of pluripotency markers POU5F1, NANOG (Nanog homeobox) and SOX2 (SRY-box 2), and upregulated the differentiation markers TUBB3 (tubulin β 3 class III), CSN2 (casein β), SPP1 (secreted phosphoprotein 1), GATA6 (GATA binding protein 6), T (T brachyury transcription factor) and CDX2 (caudal type homeobox 2). Interestingly, these pluripotency-regulating effects of NAMPT and POU5F1 were accompanied by contrasting levels of autophagy, wherein NAMPT KD promoted while POU5F1 KD inhibited the autophagy machinery. Most importantly, any deviation from the basal level of autophagy, either increase (via rapamycin, serum starvation or Tat-beclin 1 [Tat-BECN1] peptide) or decrease (via ATG7 or ATG12 KD), strongly decreased the pluripotency and promoted the differentiation and/or senescence of CSCs. Collectively, these results uncover the link between the NAD+ biosynthesis pathway, CSC transcription factor POU5F1 and pluripotency, and further identify autophagy as a novel regulator of pluripotency of CSCs.
DOI: 10.1080/15548627.2016.1260808
PubMed: 27929731
PubMed Central: PMC5324853
Links to Exploration step
pubmed:27929731Le document en format XML
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Kennedy</name><affiliation><nlm:affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Murphy, Patrick" sort="Murphy, Patrick" uniqKey="Murphy P" first="Patrick" last="Murphy">Patrick Murphy</name><affiliation><nlm:affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Clements, Derek R" sort="Clements, Derek R" uniqKey="Clements D" first="Derek R" last="Clements">Derek R. Clements</name><affiliation><nlm:affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Kim, Youra" sort="Kim, Youra" uniqKey="Kim Y" first="Youra" last="Kim">Youra Kim</name><affiliation><nlm:affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Lee, Patrick W K" sort="Lee, Patrick W K" uniqKey="Lee P" first="Patrick W K" last="Lee">Patrick W K. Lee</name><affiliation><nlm:affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Gujar, Shashi A" sort="Gujar, Shashi A" uniqKey="Gujar S" first="Shashi A" last="Gujar">Shashi A. Gujar</name><affiliation><nlm:affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation><affiliation><nlm:affiliation>c Centre for Innovative and Collaborative Health Services Research, Quality and System Performance, IWK Health Centre , Halifax , Nova Scotia , Canada.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Autophagy (drug effects)</term><term>Beclin-1 (metabolism)</term><term>Cell Differentiation (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Cell Survival (drug effects)</term><term>Cellular Senescence (drug effects)</term><term>Cytokines (antagonists & inhibitors)</term><term>Cytokines (metabolism)</term><term>Doxorubicin (pharmacology)</term><term>Homeostasis (drug effects)</term><term>Mice (MeSH)</term><term>Models, Biological (MeSH)</term><term>Neoplastic Stem Cells (drug effects)</term><term>Neoplastic Stem Cells (enzymology)</term><term>Neoplastic Stem Cells (pathology)</term><term>Nicotinamide Phosphoribosyltransferase (antagonists & inhibitors)</term><term>Nicotinamide Phosphoribosyltransferase (metabolism)</term><term>Octamer Transcription Factor-3 (metabolism)</term><term>PTEN Phosphohydrolase (metabolism)</term><term>Phosphorylation (drug effects)</term><term>Pluripotent Stem Cells (drug effects)</term><term>Pluripotent Stem Cells (pathology)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Sirolimus (pharmacology)</term><term>TOR Serine-Threonine Kinases (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cytokines</term><term>Nicotinamide Phosphoribosyltransferase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Beclin-1</term><term>Cytokines</term><term>Nicotinamide Phosphoribosyltransferase</term><term>Octamer Transcription Factor-3</term><term>PTEN Phosphohydrolase</term><term>Proto-Oncogene Proteins c-akt</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Cell Differentiation</term><term>Cell Proliferation</term><term>Cell Survival</term><term>Cellular Senescence</term><term>Homeostasis</term><term>Neoplastic Stem Cells</term><term>Phosphorylation</term><term>Pluripotent Stem Cells</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Neoplastic Stem Cells</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neoplastic Stem Cells</term><term>Pluripotent Stem Cells</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Doxorubicin</term><term>Sirolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Models, Biological</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pluripotency is an important feature of cancer stem cells (CSCs) that contributes to self-renewal and chemoresistance. The maintenance of pluripotency of CSCs under various pathophysiological conditions requires a complex interaction between various cellular pathways including those involved in homeostasis and energy metabolism. However, the exact mechanisms that maintain the CSC pluripotency remain poorly understood. In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD<sup>+</sup> synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1). First, our data show that the pharmacological inhibition and knockdown (K<sub>D</sub>) of NAMPT or the K<sub>D</sub> of POU5F1 in human CSCs significantly decreased the expression of pluripotency markers POU5F1, NANOG (Nanog homeobox) and SOX2 (SRY-box 2), and upregulated the differentiation markers TUBB3 (tubulin β 3 class III), CSN2 (casein β), SPP1 (secreted phosphoprotein 1), GATA6 (GATA binding protein 6), T (T brachyury transcription factor) and CDX2 (caudal type homeobox 2). Interestingly, these pluripotency-regulating effects of NAMPT and POU5F1 were accompanied by contrasting levels of autophagy, wherein NAMPT K<sub>D</sub> promoted while POU5F1 K<sub>D</sub> inhibited the autophagy machinery. Most importantly, any deviation from the basal level of autophagy, either increase (via rapamycin, serum starvation or Tat-beclin 1 [Tat-BECN1] peptide) or decrease (via ATG7 or ATG12 K<sub>D</sub>), strongly decreased the pluripotency and promoted the differentiation and/or senescence of CSCs. Collectively, these results uncover the link between the NAD<sup>+</sup> biosynthesis pathway, CSC transcription factor POU5F1 and pluripotency, and further identify autophagy as a novel regulator of pluripotency of CSCs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27929731</PMID><DateCompleted><Year>2017</Year><Month>11</Month><Day>28</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><Issue>2</Issue><PubDate><Year>2017</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>Autophagic homeostasis is required for the pluripotency of cancer stem cells.</ArticleTitle><Pagination><MedlinePgn>264-284</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/15548627.2016.1260808</ELocationID><Abstract><AbstractText>Pluripotency is an important feature of cancer stem cells (CSCs) that contributes to self-renewal and chemoresistance. The maintenance of pluripotency of CSCs under various pathophysiological conditions requires a complex interaction between various cellular pathways including those involved in homeostasis and energy metabolism. However, the exact mechanisms that maintain the CSC pluripotency remain poorly understood. In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD<sup>+</sup> synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1). First, our data show that the pharmacological inhibition and knockdown (K<sub>D</sub>) of NAMPT or the K<sub>D</sub> of POU5F1 in human CSCs significantly decreased the expression of pluripotency markers POU5F1, NANOG (Nanog homeobox) and SOX2 (SRY-box 2), and upregulated the differentiation markers TUBB3 (tubulin β 3 class III), CSN2 (casein β), SPP1 (secreted phosphoprotein 1), GATA6 (GATA binding protein 6), T (T brachyury transcription factor) and CDX2 (caudal type homeobox 2). Interestingly, these pluripotency-regulating effects of NAMPT and POU5F1 were accompanied by contrasting levels of autophagy, wherein NAMPT K<sub>D</sub> promoted while POU5F1 K<sub>D</sub> inhibited the autophagy machinery. Most importantly, any deviation from the basal level of autophagy, either increase (via rapamycin, serum starvation or Tat-beclin 1 [Tat-BECN1] peptide) or decrease (via ATG7 or ATG12 K<sub>D</sub>), strongly decreased the pluripotency and promoted the differentiation and/or senescence of CSCs. Collectively, these results uncover the link between the NAD<sup>+</sup> biosynthesis pathway, CSC transcription factor POU5F1 and pluripotency, and further identify autophagy as a novel regulator of pluripotency of CSCs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sharif</LastName><ForeName>Tanveer</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martell</LastName><ForeName>Emma</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dai</LastName><ForeName>Cathleen</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kennedy</LastName><ForeName>Barry E</ForeName><Initials>BE</Initials><AffiliationInfo><Affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Murphy</LastName><ForeName>Patrick</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Clements</LastName><ForeName>Derek R</ForeName><Initials>DR</Initials><AffiliationInfo><Affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Youra</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Patrick W K</ForeName><Initials>PW</Initials><AffiliationInfo><Affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gujar</LastName><ForeName>Shashi A</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>a Department of Microbiology and Immunology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>b Department of Pathology , Dalhousie University , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>c Centre for Innovative and Collaborative Health Services Research, Quality and System Performance, IWK Health Centre , Halifax , Nova Scotia , Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>12</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Autophagy</MedlineTA><NlmUniqueID>101265188</NlmUniqueID><ISSNLinking>1554-8627</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000071186">Beclin-1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050814">Octamer Transcription Factor-3</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C494173">POU5F1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>80168379AG</RegistryNumber><NameOfSubstance UI="D004317">Doxorubicin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.4.2.12</RegistryNumber><NameOfSubstance UI="D054409">Nicotinamide Phosphoribosyltransferase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.4.2.12</RegistryNumber><NameOfSubstance UI="C085455">nicotinamide phosphoribosyltransferase, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.67</RegistryNumber><NameOfSubstance UI="D051059">PTEN Phosphohydrolase</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016922" MajorTopicYN="N">Cellular Senescence</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004317" MajorTopicYN="N">Doxorubicin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006706" MajorTopicYN="Y">Homeostasis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014411" MajorTopicYN="N">Neoplastic Stem Cells</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054409" MajorTopicYN="N">Nicotinamide Phosphoribosyltransferase</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050814" MajorTopicYN="N">Octamer Transcription Factor-3</DescriptorName><QualifierName UI="Q000378" 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PubStatus="entrez"><Year>2016</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27929731</ArticleId><ArticleId IdType="doi">10.1080/15548627.2016.1260808</ArticleId><ArticleId IdType="pmc">PMC5324853</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Cell Cycle. 2007 Aug 1;6(15):1837-49</Citation><ArticleIdList><ArticleId IdType="pubmed">17671424</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell. 2012 Nov 30;48(4):627-40</Citation><ArticleIdList><ArticleId IdType="pubmed">23041284</ArticleId></ArticleIdList></Reference><Reference><Citation>Annu Rev Genet. 2009;43:67-93</Citation><ArticleIdList><ArticleId IdType="pubmed">19653858</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2013 Feb 14;494(7436):201-6</Citation><ArticleIdList><ArticleId IdType="pubmed">23364696</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2004 Aug 15;18(16):1926-45</Citation><ArticleIdList><ArticleId IdType="pubmed">15314020</ArticleId></ArticleIdList></Reference><Reference><Citation>Genes Dev. 2007 Nov 15;21(22):2861-73</Citation><ArticleIdList><ArticleId IdType="pubmed">18006683</ArticleId></ArticleIdList></Reference><Reference><Citation>Immunol Invest. 2005;34(2):215-36</Citation><ArticleIdList><ArticleId IdType="pubmed">15921160</ArticleId></ArticleIdList></Reference><Reference><Citation>Cancer Lett. 2009 May 8;277(1):1-7</Citation><ArticleIdList><ArticleId IdType="pubmed">18809245</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Cancer. 2007 Dec;7(12 ):961-7</Citation><ArticleIdList><ArticleId IdType="pubmed">17972889</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2016 Jan 7;529(7584):37-42</Citation><ArticleIdList><ArticleId IdType="pubmed">26738589</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 1994 Feb 17;367(6464):645-8</Citation><ArticleIdList><ArticleId IdType="pubmed">7509044</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Med. 2011 Mar;17(3):313-9</Citation><ArticleIdList><ArticleId IdType="pubmed">21386835</ArticleId></ArticleIdList></Reference><Reference><Citation>J Clin Invest. 2015 Jan;125(1):14-24</Citation><ArticleIdList><ArticleId IdType="pubmed">25654546</ArticleId></ArticleIdList></Reference><Reference><Citation>Invest New Drugs. 2011 Apr;29(2):239-47</Citation><ArticleIdList><ArticleId IdType="pubmed">19943082</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Stem Cell. 2014 Mar 6;14(3):275-91</Citation><ArticleIdList><ArticleId IdType="pubmed">24607403</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cancer Ther. 2010 Nov;9(11):2924-33</Citation><ArticleIdList><ArticleId IdType="pubmed">20978162</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2007 Jan 4;445(7123):106-10</Citation><ArticleIdList><ArticleId IdType="pubmed">17122772</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Tissue Res. 2012 Nov;350(2):361-72</Citation><ArticleIdList><ArticleId IdType="pubmed">22864983</ArticleId></ArticleIdList></Reference><Reference><Citation>J Natl Cancer Inst. 2010 Oct 20;102(20):1536-46</Citation><ArticleIdList><ArticleId IdType="pubmed">20858887</ArticleId></ArticleIdList></Reference><Reference><Citation>J Biol Chem. 2005 Jul 1;280(26):24731-7</Citation><ArticleIdList><ArticleId IdType="pubmed">15860457</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Protoc. 2009;4(12):1798-806</Citation><ArticleIdList><ArticleId IdType="pubmed">20010931</ArticleId></ArticleIdList></Reference><Reference><Citation>J Neurosci. 1996 Feb 1;16(3):1056-65</Citation><ArticleIdList><ArticleId IdType="pubmed">8558234</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2006 Aug 25;126(4):663-76</Citation><ArticleIdList><ArticleId IdType="pubmed">16904174</ArticleId></ArticleIdList></Reference><Reference><Citation>Dev Biol. 1995 Apr;168(2):342-57</Citation><ArticleIdList><ArticleId IdType="pubmed">7729574</ArticleId></ArticleIdList></Reference><Reference><Citation>Trends Endocrinol Metab. 2009 Apr;20(3):130-8</Citation><ArticleIdList><ArticleId IdType="pubmed">19109034</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Stem Cell. 2013 Jan 3;12(1):88-100</Citation><ArticleIdList><ArticleId IdType="pubmed">23260487</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Rev Drug Discov. 2009 Oct;8(10):806-23</Citation><ArticleIdList><ArticleId IdType="pubmed">19794444</ArticleId></ArticleIdList></Reference><Reference><Citation>Blood. 2012 Oct 25;120(17):3519-29</Citation><ArticleIdList><ArticleId IdType="pubmed">22955917</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Genet. 2000 Apr;24(4):372-6</Citation><ArticleIdList><ArticleId IdType="pubmed">10742100</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2016;12 (1):1-222</Citation><ArticleIdList><ArticleId IdType="pubmed">26799652</ArticleId></ArticleIdList></Reference><Reference><Citation>Discov Med. 2005 Jun;5(27):278-82</Citation><ArticleIdList><ArticleId IdType="pubmed">20704888</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2003 May 15;423(6937):302-5</Citation><ArticleIdList><ArticleId IdType="pubmed">12714971</ArticleId></ArticleIdList></Reference><Reference><Citation>Free Radic Biol Med. 2011 Dec 1;51(11):2007-17</Citation><ArticleIdList><ArticleId IdType="pubmed">21945098</ArticleId></ArticleIdList></Reference><Reference><Citation>Biochem Pharmacol. 2013 Jan 1;85(1):124-34</Citation><ArticleIdList><ArticleId IdType="pubmed">23107818</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell Death Differ. 2016 Apr;23 (4):669-80</Citation><ArticleIdList><ArticleId IdType="pubmed">26586573</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 2005 Jul;25(14):6031-46</Citation><ArticleIdList><ArticleId IdType="pubmed">15988017</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 2010 Nov 12;143(4):508-25</Citation><ArticleIdList><ArticleId IdType="pubmed">21074044</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Cell Biol. 2011 May;13(5):490-6</Citation><ArticleIdList><ArticleId IdType="pubmed">21540844</ArticleId></ArticleIdList></Reference><Reference><Citation>Nature. 2007 Jan 4;445(7123):111-5</Citation><ArticleIdList><ArticleId IdType="pubmed">17122771</ArticleId></ArticleIdList></Reference><Reference><Citation>Stem Cells Int. 2015;2015:369828</Citation><ArticleIdList><ArticleId IdType="pubmed">26089914</ArticleId></ArticleIdList></Reference><Reference><Citation>Proc Natl Acad Sci U S A. 2010 Jan 26;107(4):1402-7</Citation><ArticleIdList><ArticleId IdType="pubmed">20080709</ArticleId></ArticleIdList></Reference><Reference><Citation>Cell. 1998 Oct 30;95(3):379-91</Citation><ArticleIdList><ArticleId IdType="pubmed">9814708</ArticleId></ArticleIdList></Reference><Reference><Citation>Nat Med. 2006 Mar;12(3):296-300</Citation><ArticleIdList><ArticleId IdType="pubmed">16520777</ArticleId></ArticleIdList></Reference><Reference><Citation>Autophagy. 2008 Apr;4(3):385-7</Citation><ArticleIdList><ArticleId IdType="pubmed">18227641</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Cell Biol. 2005 Jul;25(14 ):6211-24</Citation><ArticleIdList><ArticleId IdType="pubmed">15988030</ArticleId></ArticleIdList></Reference><Reference><Citation>Mol Med Rep. 2014 May;9(5):1975-81</Citation><ArticleIdList><ArticleId 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