CDK5RAP3 Participates in Autophagy Regulation and Is Downregulated in Renal Cancer
Identifieur interne : 000600 ( Ncbi/Merge ); précédent : 000599; suivant : 000601CDK5RAP3 Participates in Autophagy Regulation and Is Downregulated in Renal Cancer
Auteurs : Jun Li [République populaire de Chine] ; Xinyi Hu [République populaire de Chine] ; Ming Su [République populaire de Chine] ; Hongliang Shen [République populaire de Chine] ; Wei Qiu [République populaire de Chine] ; Ye Tian [République populaire de Chine]Source :
- Disease Markers [ 0278-0240 ] ; 2019.
Abstract
Renal cancer is one of the most common malignant urological tumors; however, its diagnosis and treatment are not well established. In the present study, we identified that CDK5 regulatory subunit-associated protein 3 (CDK5RAP3), a putative tumor suppressor in many cancers, was downregulated in renal cancer tissues. Through loss- and gain-of-function experiments, we observed that the action of CDK5RAP3 in renal cancer cells was different in Caki-1 and 769-P cell lines. Knockdown of endogenous CDK5RAP3 in Caki-1 slightly increased cell viability, whereas overexpression of CDK5RAP3 in 769-P cells inhibited cell viability. In addition, we observed that CDK5RAP3 participated in the regulation of autophagy in renal cancer. Knockdown of CDK5RAP3 induced significant inhibition of autophagy in Caki-1 cells but not in 769-P cells. In contrast, overexpression of CDK5RAP3 significantly activated autophagy in 769-P cells, as evidenced by increased LC3-II levels. However, the LC3-II could not be altered by CDK5RAP3 overexpression in Caki-1 cells. These findings demonstrated that CDK5RAP3 is downregulated in renal cancer and may be associated with autophagy.
Url:
DOI: 10.1155/2019/6171782
PubMed: 31061682
PubMed Central: 6466961
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Hu</name><affiliation wicri:level="3"><nlm:aff id="I1">Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Su, Ming" sort="Su, Ming" uniqKey="Su M" first="Ming" last="Su">Ming Su</name><affiliation wicri:level="3"><nlm:aff id="I2">Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Clinical Laboratory, Peking University People's Hospital, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Shen, Hongliang" sort="Shen, Hongliang" uniqKey="Shen H" first="Hongliang" last="Shen">Hongliang Shen</name><affiliation wicri:level="3"><nlm:aff id="I1">Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Qiu, Wei" sort="Qiu, Wei" uniqKey="Qiu W" first="Wei" last="Qiu">Wei Qiu</name><affiliation wicri:level="3"><nlm:aff id="I1">Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Tian, Ye" sort="Tian, Ye" uniqKey="Tian Y" first="Ye" last="Tian">Ye Tian</name><affiliation wicri:level="3"><nlm:aff id="I1">Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author></analytic><series><title level="j">Disease Markers</title><idno type="ISSN">0278-0240</idno><idno type="eISSN">1875-8630</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>Renal cancer is one of the most common malignant urological tumors; however, its diagnosis and treatment are not well established. In the present study, we identified that CDK5 regulatory subunit-associated protein 3 (CDK5RAP3), a putative tumor suppressor in many cancers, was downregulated in renal cancer tissues. Through loss- and gain-of-function experiments, we observed that the action of CDK5RAP3 in renal cancer cells was different in Caki-1 and 769-P cell lines. Knockdown of endogenous CDK5RAP3 in Caki-1 slightly increased cell viability, whereas overexpression of CDK5RAP3 in 769-P cells inhibited cell viability. In addition, we observed that CDK5RAP3 participated in the regulation of autophagy in renal cancer. Knockdown of CDK5RAP3 induced significant inhibition of autophagy in Caki-1 cells but not in 769-P cells. In contrast, overexpression of CDK5RAP3 significantly activated autophagy in 769-P cells, as evidenced by increased LC3-II levels. However, the LC3-II could not be altered by CDK5RAP3 overexpression in Caki-1 cells. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Dis Markers</journal-id><journal-id journal-id-type="iso-abbrev">Dis. Markers</journal-id><journal-id journal-id-type="publisher-id">DM</journal-id><journal-title-group><journal-title>Disease Markers</journal-title></journal-title-group><issn pub-type="ppub">0278-0240</issn><issn pub-type="epub">1875-8630</issn><publisher><publisher-name>Hindawi</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31061682</article-id><article-id pub-id-type="pmc">6466961</article-id><article-id pub-id-type="doi">10.1155/2019/6171782</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>CDK5RAP3 Participates in Autophagy Regulation and Is Downregulated in Renal Cancer</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-2290-6087</contrib-id><name><surname>Li</surname><given-names>Jun</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0001-5873-8276</contrib-id><name><surname>Hu</surname><given-names>Xinyi</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-0252-7936</contrib-id><name><surname>Su</surname><given-names>Ming</given-names></name><xref ref-type="aff" rid="I2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0001-9110-6326</contrib-id><name><surname>Shen</surname><given-names>Hongliang</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-0188-4931</contrib-id><name><surname>Qiu</surname><given-names>Wei</given-names></name><email>qiuwei618@163.com</email><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0001-8523-9683</contrib-id><name><surname>Tian</surname><given-names>Ye</given-names></name><email>youyiminiao@126.com</email><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib></contrib-group><aff id="I1"><sup>1</sup>Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing, China</aff><aff id="I2"><sup>2</sup>Department of Clinical Laboratory, Peking University People's Hospital, Beijing, China</aff><author-notes><fn fn-type="other"><p>Academic Editor: Anja Hviid Simonsen</p></fn></author-notes><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>2</day><month>4</month><year>2019</year></pub-date><volume>2019</volume><elocation-id>6171782</elocation-id><history><date date-type="received"><day>14</day><month>11</month><year>2018</year></date><date date-type="rev-recd"><day>5</day><month>1</month><year>2019</year></date><date date-type="accepted"><day>5</day><month>2</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 Jun Li et al.</copyright-statement><copyright-year>2019</copyright-year><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>Renal cancer is one of the most common malignant urological tumors; however, its diagnosis and treatment are not well established. In the present study, we identified that CDK5 regulatory subunit-associated protein 3 (CDK5RAP3), a putative tumor suppressor in many cancers, was downregulated in renal cancer tissues. Through loss- and gain-of-function experiments, we observed that the action of CDK5RAP3 in renal cancer cells was different in Caki-1 and 769-P cell lines. Knockdown of endogenous CDK5RAP3 in Caki-1 slightly increased cell viability, whereas overexpression of CDK5RAP3 in 769-P cells inhibited cell viability. In addition, we observed that CDK5RAP3 participated in the regulation of autophagy in renal cancer. Knockdown of CDK5RAP3 induced significant inhibition of autophagy in Caki-1 cells but not in 769-P cells. In contrast, overexpression of CDK5RAP3 significantly activated autophagy in 769-P cells, as evidenced by increased LC3-II levels. However, the LC3-II could not be altered by CDK5RAP3 overexpression in Caki-1 cells. These findings demonstrated that CDK5RAP3 is downregulated in renal cancer and may be associated with autophagy.</p></abstract><funding-group><award-group><funding-source>National Natural Science Foundation of China</funding-source><award-id>81602214</award-id></award-group></funding-group></article-meta></front><floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label><caption><p>CDK5RAP3 is downregulated in renal cancer. (a) Immunohistochemical staining of CDK5RAP3 was performed in renal cancerous (RCT) and paracancerous (PCT) tissues. Representative images are shown. (b, c) The protein level of CDK5RAP3 was detected by western blotting (b). GAPDH was employed as an internal control, and representative images are shown (<italic>n</italic> = 25; C: cancerous tissue, P: paracancerous tissue). The relative expression intensity of CDK5RAP3 was measured, and a Mann-Whitney <italic>U</italic> test was used for analyzing differences between RCT and PCT.</p></caption><graphic xlink:href="DM2019-6171782.001"></graphic></fig><fig id="fig2" orientation="portrait" position="float"><label>Figure 2</label><caption><p>CDK5RAP3 inhibits renal cancer cell viability. (a) The expression of CDK5RAP3 in Caki-1 and 769-P cells is shown. (b, c) Caki-1 (a) and 769-P (b) cells were transfected with siRNAs targeting CDK5RAP3 with two different sequences (seq1 and seq2) for knockdown or were infected with adenoviruses carrying CDK5RAP3 for overexpression. CCK-8 assays were performed to measure cell viability. Data are expressed as mean ± standard deviation, <italic>n</italic> = 6 per group.</p></caption><graphic xlink:href="DM2019-6171782.002"></graphic></fig><fig id="fig3" orientation="portrait" position="float"><label>Figure 3</label><caption><p>CDK5RAP3 regulates autophagy in renal cancer cells. (a, b) Endogenous CDK5RAP3 in Caki-1 and 769-P cells was infected with adenoviral vectors carrying CDK5RAP3 for overexpression (a) or knocked down (b) with two specific siRNAs (seq1 and seq2). The conversion of LC3 was detected using western blotting.</p></caption><graphic xlink:href="DM2019-6171782.003"></graphic></fig></floats-group></pmc><affiliations><list><country><li>République populaire de Chine</li></country><settlement><li>Pékin</li></settlement></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Li, Jun" sort="Li, Jun" uniqKey="Li J" first="Jun" last="Li">Jun Li</name></noRegion><name sortKey="Hu, Xinyi" sort="Hu, Xinyi" uniqKey="Hu X" first="Xinyi" last="Hu">Xinyi Hu</name><name sortKey="Qiu, Wei" sort="Qiu, Wei" uniqKey="Qiu W" first="Wei" last="Qiu">Wei Qiu</name><name sortKey="Shen, Hongliang" sort="Shen, Hongliang" uniqKey="Shen H" first="Hongliang" last="Shen">Hongliang Shen</name><name sortKey="Su, Ming" sort="Su, Ming" uniqKey="Su M" first="Ming" last="Su">Ming Su</name><name sortKey="Tian, Ye" sort="Tian, Ye" uniqKey="Tian Y" first="Ye" last="Tian">Ye Tian</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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