ATG3, a Target of miR-431-5p, Promotes Proliferation and Invasion of Colon Cancer via Promoting Autophagy
Identifieur interne : 000D30 ( Ncbi/Merge ); précédent : 000D29; suivant : 000D31ATG3, a Target of miR-431-5p, Promotes Proliferation and Invasion of Colon Cancer via Promoting Autophagy
Auteurs : Wei Huang [République populaire de Chine] ; Chong Zeng [République populaire de Chine] ; Shanbiao Hu [République populaire de Chine] ; Lei Wang [République populaire de Chine] ; Jie Liu [République populaire de Chine]Source :
- Cancer Management and Research [ 1179-1322 ] ; 2019.
Abstract
Studies have indicated that ATG3 could mediate the effects of other tumor-related regulators in carcinogenesis. However, the expression, role, and mechanism of ATG3 itself in cancers are rarely revealed. Thus, we explored the expression, function, and mechanism of ATG3 in colon cancer.
The expression of ATG3 was detected in colon cancer tissues and cell lines, as well as in adjacent tumor tissues and normal colon epithelial cells. The effects of ATG3 alteration on proliferation and invasion were further analyzed. The expression and role of miR-431-5p, a potential negative regulator of ATG3, were also studied. Eventually, the role of autophagy in ATG3 related effects in colon cancer was checked.
ATG3 is upregulated in colon cancer tissues and cells demonstrated by qPCR and IHC. ATG3 knockdown significantly suppressed proliferation and invasion of colon cancer cells indicated by plate clone formation and Transwell invasion assays. The expression of miR-431-5p is downregulated and negatively correlates with ATG3 in colon cancer. Furthermore, luciferase report system, plate clone formation and Transwell invasion assays demonstrated that miR-431-5p could prohibit cell proliferation and invasion via directly targeting ATG3 in colon cancer. Eventually, Western blot, plate clone formation and Transwell invasion assays proved that autophagy block could antagonize the promotive functions of ATG3 on proliferation and invasion in cancer suggesting autophagy activation accounts for the promotive role of ATG3 on proliferation and invasion in colon cancer.
Collectively, ATG3 upregulation, caused by downregulated miR-435-5p, promotes proliferation and invasion via an autophagy-dependent manner in colon cancer suggesting that miR-431-5p/ATG3/autophagy may be a potential therapeutic target in colon cancer.
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DOI: 10.2147/CMAR.S226828
PubMed: 31849517
PubMed Central: 6911302
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Therapy, Xiangya Hospital, Central South University</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Zeng, Chong" sort="Zeng, Chong" uniqKey="Zeng C" first="Chong" last="Zeng">Chong Zeng</name><affiliation wicri:level="1"><nlm:aff id="AFF0003"><institution>Department of Respiratory and Neurology, Hunan Rongjun Hospital</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Hu, Shanbiao" sort="Hu, Shanbiao" uniqKey="Hu S" first="Shanbiao" last="Hu">Shanbiao Hu</name><affiliation wicri:level="1"><nlm:aff id="AFF0004"><institution>Department of Urological Organ Transplantation, The Second Xiangya Hospital of Central South University</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Wang, Lei" sort="Wang, Lei" uniqKey="Wang L" first="Lei" last="Wang">Lei Wang</name><affiliation wicri:level="1"><nlm:aff id="AFF0005"><institution>Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Liu, Jie" sort="Liu, Jie" uniqKey="Liu J" first="Jie" last="Liu">Jie Liu</name><affiliation wicri:level="1"><nlm:aff id="AFF0001"><institution>Department of Pathology, Changsha Central Hospital</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cancer Management and Research</title><idno type="eISSN">1179-1322</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S2001"><title>Background</title><p>Studies have indicated that ATG3 could mediate the effects of other tumor-related regulators in carcinogenesis. However, the expression, role, and mechanism of ATG3 itself in cancers are rarely revealed. Thus, we explored the expression, function, and mechanism of ATG3 in colon cancer.</p></sec><sec id="S2002"><title>Materials and methods</title><p>The expression of ATG3 was detected in colon cancer tissues and cell lines, as well as in adjacent tumor tissues and normal colon epithelial cells. The effects of ATG3 alteration on proliferation and invasion were further analyzed. The expression and role of miR-431-5p, a potential negative regulator of ATG3, were also studied. Eventually, the role of autophagy in ATG3 related effects in colon cancer was checked.</p></sec><sec id="S2003"><title>Results</title><p>ATG3 is upregulated in colon cancer tissues and cells demonstrated by qPCR and IHC. ATG3 knockdown significantly suppressed proliferation and invasion of colon cancer cells indicated by plate clone formation and Transwell invasion assays. The expression of miR-431-5p is downregulated and negatively correlates with ATG3 in colon cancer. Furthermore, luciferase report system, plate clone formation and Transwell invasion assays demonstrated that miR-431-5p could prohibit cell proliferation and invasion via directly targeting ATG3 in colon cancer. Eventually, Western blot, plate clone formation and Transwell invasion assays proved that autophagy block could antagonize the promotive functions of ATG3 on proliferation and invasion in cancer suggesting autophagy activation accounts for the promotive role of ATG3 on proliferation and invasion in colon cancer.</p></sec><sec id="S2004"><title>Conclusion</title><p>Collectively, ATG3 upregulation, caused by downregulated miR-435-5p, promotes proliferation and invasion via an autophagy-dependent manner in colon cancer suggesting that miR-431-5p/ATG3/autophagy may be a potential therapeutic target in colon cancer.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cancer Manag Res</journal-id><journal-id journal-id-type="iso-abbrev">Cancer Manag Res</journal-id><journal-id journal-id-type="publisher-id">CMAR</journal-id><journal-id journal-id-type="pmc">cancmanres</journal-id><journal-title-group><journal-title>Cancer Management and Research</journal-title></journal-title-group><issn pub-type="epub">1179-1322</issn><publisher><publisher-name>Dove</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31849517</article-id><article-id pub-id-type="pmc">6911302</article-id><article-id pub-id-type="publisher-id">226828</article-id><article-id pub-id-type="doi">10.2147/CMAR.S226828</article-id><article-categories><subj-group subj-group-type="heading"><subject>Original Research</subject></subj-group></article-categories><title-group><article-title>ATG3, a Target of miR-431-5p, Promotes Proliferation and Invasion of Colon Cancer via Promoting Autophagy</article-title><alt-title alt-title-type="running-authors">Huang et al</alt-title><alt-title alt-title-type="running-title">Huang et al</alt-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Huang</surname><given-names>Wei</given-names></name><xref ref-type="aff" rid="AFF0001">1</xref><xref ref-type="aff" rid="AFF0002">2</xref></contrib><contrib contrib-type="author"><name><surname>Zeng</surname><given-names>Chong</given-names></name><xref ref-type="aff" rid="AFF0003">3</xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="false">http://orcid.org/0000-0002-1520-9531</contrib-id><name><surname>Hu</surname><given-names>Shanbiao</given-names></name><xref ref-type="aff" rid="AFF0004">4</xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Lei</given-names></name><xref ref-type="aff" rid="AFF0005">5</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Jie</given-names></name><xref ref-type="corresp" rid="AN0001"></xref><xref ref-type="aff" rid="AFF0001">1</xref></contrib><aff id="AFF0001"><label>1</label><institution>Department of Pathology, Changsha Central Hospital</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></aff><aff id="AFF0002"><label>2</label><institution>Research Center of Carcinogenesis and Targeted Therapy, Xiangya Hospital, Central South University</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></aff><aff id="AFF0003"><label>3</label><institution>Department of Respiratory and Neurology, Hunan Rongjun Hospital</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></aff><aff id="AFF0004"><label>4</label><institution>Department of Urological Organ Transplantation, The Second Xiangya Hospital of Central South University</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></aff><aff id="AFF0005"><label>5</label><institution>Cancer Research Institute, Collaborative Innovation Center for Cancer Medicine, School of Basic Medical Science, Central South University</institution>,<addr-line>Changsha</addr-line>,<addr-line>Hunan</addr-line>,<country>People’s Republic of China</country></aff></contrib-group><author-notes><corresp id="AN0001">Correspondence: Jie Liu <institution>Department of Pathology, Changsha Central Hospital</institution>, <addr-line>No. 161 Shaoshan South Road</addr-line>, <addr-line>Changsha</addr-line>, <addr-line>Hunan</addr-line><addr-line>410004</addr-line>, <country>People’s Republic of China</country> Email lj511907352@163.com</corresp></author-notes><pub-date pub-type="epub"><day>09</day><month>12</month><year>2019</year></pub-date><pub-date pub-type="collection"><year>2019</year></pub-date><volume>11</volume><fpage>10275</fpage><lpage>10285</lpage><history><date date-type="received"><day>11</day><month>8</month><year>2019</year></date><date date-type="accepted"><day>12</day><month>11</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 Huang et al.</copyright-statement><copyright-year>2019</copyright-year><copyright-holder>Huang et al.</copyright-holder><license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/"><license-p>This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at <ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link> and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc/3.0/">http://creativecommons.org/licenses/by-nc/3.0/</ext-link>). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (<ext-link ext-link-type="uri" xlink:href="https://www.dovepress.com/terms.php">https://www.dovepress.com/terms.php</ext-link>).</license-p></license></permissions><abstract><sec id="S2001"><title>Background</title><p>Studies have indicated that ATG3 could mediate the effects of other tumor-related regulators in carcinogenesis. However, the expression, role, and mechanism of ATG3 itself in cancers are rarely revealed. Thus, we explored the expression, function, and mechanism of ATG3 in colon cancer.</p></sec><sec id="S2002"><title>Materials and methods</title><p>The expression of ATG3 was detected in colon cancer tissues and cell lines, as well as in adjacent tumor tissues and normal colon epithelial cells. The effects of ATG3 alteration on proliferation and invasion were further analyzed. The expression and role of miR-431-5p, a potential negative regulator of ATG3, were also studied. Eventually, the role of autophagy in ATG3 related effects in colon cancer was checked.</p></sec><sec id="S2003"><title>Results</title><p>ATG3 is upregulated in colon cancer tissues and cells demonstrated by qPCR and IHC. ATG3 knockdown significantly suppressed proliferation and invasion of colon cancer cells indicated by plate clone formation and Transwell invasion assays. The expression of miR-431-5p is downregulated and negatively correlates with ATG3 in colon cancer. Furthermore, luciferase report system, plate clone formation and Transwell invasion assays demonstrated that miR-431-5p could prohibit cell proliferation and invasion via directly targeting ATG3 in colon cancer. Eventually, Western blot, plate clone formation and Transwell invasion assays proved that autophagy block could antagonize the promotive functions of ATG3 on proliferation and invasion in cancer suggesting autophagy activation accounts for the promotive role of ATG3 on proliferation and invasion in colon cancer.</p></sec><sec id="S2004"><title>Conclusion</title><p>Collectively, ATG3 upregulation, caused by downregulated miR-435-5p, promotes proliferation and invasion via an autophagy-dependent manner in colon cancer suggesting that miR-431-5p/ATG3/autophagy may be a potential therapeutic target in colon cancer.</p></sec></abstract><kwd-group kwd-group-type="author"><title>Keywords</title><kwd>colon cancer</kwd><kwd>proliferation</kwd><kwd>invasion</kwd><kwd>ATG3</kwd><kwd>miR-431-5p</kwd><kwd>autophagy</kwd></kwd-group><counts><fig-count count="5"></fig-count><ref-count count="40"></ref-count><page-count count="11"></page-count></counts></article-meta></front></pmc><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Huang, Wei" sort="Huang, Wei" uniqKey="Huang W" first="Wei" last="Huang">Wei Huang</name></noRegion><name sortKey="Hu, Shanbiao" sort="Hu, Shanbiao" uniqKey="Hu S" first="Shanbiao" last="Hu">Shanbiao Hu</name><name sortKey="Huang, Wei" sort="Huang, Wei" uniqKey="Huang W" first="Wei" last="Huang">Wei Huang</name><name sortKey="Liu, Jie" sort="Liu, Jie" uniqKey="Liu J" first="Jie" last="Liu">Jie Liu</name><name sortKey="Wang, Lei" sort="Wang, Lei" uniqKey="Wang L" first="Lei" last="Wang">Lei Wang</name><name sortKey="Zeng, Chong" sort="Zeng, Chong" uniqKey="Zeng C" first="Chong" last="Zeng">Chong Zeng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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