ERas Enhances Resistance to Cisplatin-Induced Apoptosis by Suppressing Autophagy in Gastric Cancer Cell
Identifieur interne : 000157 ( Pmc/Checkpoint ); précédent : 000156; suivant : 000158ERas Enhances Resistance to Cisplatin-Induced Apoptosis by Suppressing Autophagy in Gastric Cancer Cell
Auteurs : Huajian Tian [République populaire de Chine] ; Wenjun Wang [République populaire de Chine] ; Xiao Meng [République populaire de Chine] ; Miaomiao Wang [République populaire de Chine] ; Junyang Tan [République populaire de Chine] ; Wenjuan Jia [République populaire de Chine] ; Peining Li [États-Unis] ; Jianshuang Li [République populaire de Chine] ; Qinghua Zhou [République populaire de Chine]Source :
- Frontiers in Cell and Developmental Biology [ 2296-634X ] ; 2020.
Abstract
Gastric cancer (GC), a common type of malignant cancer, remains the fifth most frequently diagnosed cancer and the third leading cause of cancer-related deaths worldwide. Despite developments in the treatment of GC, the prognosis remains poor. Embryonic stem cell-expressed Ras (ERas), a novel member of the Ras protein family, has recently been identified as an oncogene involved in the tumorigenic growth of embryonic stem cells. A recent study reported that ERas is expressed in most GC cell lines and GC specimens, and it promotes tumorigenicity in GC through induction of the epithelial mesenchymal transition (EMT) and activation of the PI3K/AKT pathway. Here, we found that ERas blocked autophagy flux in BGC-823 and AGS GC cells, which may occur through activation of the AKT/mTOR signaling pathway. Moreover, ERas overexpression suppressed cisplatin-induced apoptosis, and rapamycin treatment significantly attenuated ERas-mediated cisplatin resistance in GC cells. These data suggest that ERas may be a potential therapeutic target to improve the outcomes of GC patients by regulating the autophagy process.
Url:
DOI: 10.3389/fcell.2019.00375
PubMed: 32083074
PubMed Central: 7005724
Affiliations:
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University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Meng, Xiao" sort="Meng, Xiao" uniqKey="Meng X" first="Xiao" last="Meng">Xiao Meng</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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, Miaomiao" sort="Wang, Miaomiao" uniqKey="Wang M" first="Miaomiao" last="Wang">Miaomiao Wang</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Tan, Junyang" sort="Tan, Junyang" uniqKey="Tan J" first="Junyang" last="Tan">Junyang Tan</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Jia, Wenjuan" sort="Jia, Wenjuan" uniqKey="Jia W" first="Wenjuan" last="Jia">Wenjuan Jia</name><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Qingyuan People’s Hospital, The Sixth Affiliated Hospital of Guangzhou Medical University</institution>,<addr-line>Qingyuan</addr-line>,<country>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="Li, Peining" sort="Li, Peining" uniqKey="Li P" first="Peining" last="Li">Peining Li</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Department of Genetics, Yale School of Medicine, Yale University</institution>,<addr-line>New Haven, CT</addr-line>,<country>United States</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Li, Jianshuang" sort="Li, Jianshuang" uniqKey="Li J" first="Jianshuang" last="Li">Jianshuang Li</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Zhou, Qinghua" sort="Zhou, Qinghua" uniqKey="Zhou Q" first="Qinghua" last="Zhou">Qinghua Zhou</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>China</country></nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">32083074</idno><idno type="pmc">7005724</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7005724</idno><idno type="RBID">PMC:7005724</idno><idno type="doi">10.3389/fcell.2019.00375</idno><date when="2020">2020</date><idno type="wicri:Area/Pmc/Corpus">000528</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000528</idno><idno type="wicri:Area/Pmc/Curation">000528</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000528</idno><idno type="wicri:Area/Pmc/Checkpoint">000157</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000157</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">ERas Enhances Resistance to Cisplatin-Induced Apoptosis by Suppressing Autophagy in Gastric Cancer Cell</title><author><name sortKey="Tian, Huajian" sort="Tian, Huajian" uniqKey="Tian H" first="Huajian" last="Tian">Huajian Tian</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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, Wenjun" sort="Wang, Wenjun" uniqKey="Wang W" first="Wenjun" last="Wang">Wenjun Wang</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Meng, Xiao" sort="Meng, Xiao" uniqKey="Meng X" first="Xiao" last="Meng">Xiao Meng</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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, Miaomiao" sort="Wang, Miaomiao" uniqKey="Wang M" first="Miaomiao" last="Wang">Miaomiao Wang</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Tan, Junyang" sort="Tan, Junyang" uniqKey="Tan J" first="Junyang" last="Tan">Junyang Tan</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Jia, Wenjuan" sort="Jia, Wenjuan" uniqKey="Jia W" first="Wenjuan" last="Jia">Wenjuan Jia</name><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Qingyuan People’s Hospital, The Sixth Affiliated Hospital of Guangzhou Medical University</institution>,<addr-line>Qingyuan</addr-line>,<country>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="Li, Peining" sort="Li, Peining" uniqKey="Li P" first="Peining" last="Li">Peining Li</name><affiliation wicri:level="1"><nlm:aff id="aff3"><institution>Department of Genetics, Yale School of Medicine, Yale University</institution>,<addr-line>New Haven, CT</addr-line>,<country>United States</country></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea># see nlm:aff country strict</wicri:regionArea></affiliation></author><author><name sortKey="Li, Jianshuang" sort="Li, Jianshuang" uniqKey="Li J" first="Jianshuang" last="Li">Jianshuang Li</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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="Zhou, Qinghua" sort="Zhou, Qinghua" uniqKey="Zhou Q" first="Qinghua" last="Zhou">Qinghua Zhou</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>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">Frontiers in Cell and Developmental Biology</title><idno type="eISSN">2296-634X</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Gastric cancer (GC), a common type of malignant cancer, remains the fifth most frequently diagnosed cancer and the third leading cause of cancer-related deaths worldwide. Despite developments in the treatment of GC, the prognosis remains poor. Embryonic stem cell-expressed Ras (ERas), a novel member of the Ras protein family, has recently been identified as an oncogene involved in the tumorigenic growth of embryonic stem cells. A recent study reported that ERas is expressed in most GC cell lines and GC specimens, and it promotes tumorigenicity in GC through induction of the epithelial mesenchymal transition (EMT) and activation of the PI3K/AKT pathway. Here, we found that ERas blocked autophagy flux in BGC-823 and AGS GC cells, which may occur through activation of the AKT/mTOR signaling pathway. Moreover, ERas overexpression suppressed cisplatin-induced apoptosis, and rapamycin treatment significantly attenuated ERas-mediated cisplatin resistance in GC cells. These data suggest that ERas may be a potential therapeutic target to improve the outcomes of GC patients by regulating the autophagy process.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Aoyama, M" uniqKey="Aoyama M">M. Aoyama</name></author><author><name sortKey="Kataoka, H" uniqKey="Kataoka H">H. Kataoka</name></author><author><name sortKey="Kubota, E" uniqKey="Kubota E">E. Kubota</name></author><author><name sortKey="Tada, T" uniqKey="Tada T">T. Tada</name></author><author><name sortKey="Asai, K" uniqKey="Asai K">K. Asai</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bray, F" uniqKey="Bray F">F. Bray</name></author><author><name sortKey="Ferlay, J" uniqKey="Ferlay J">J. Ferlay</name></author><author><name sortKey="Soerjomataram, I" uniqKey="Soerjomataram I">I. Soerjomataram</name></author><author><name sortKey="Siegel, R L" uniqKey="Siegel R">R. L. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Cell Dev Biol</journal-id><journal-id journal-id-type="iso-abbrev">Front Cell Dev Biol</journal-id><journal-id journal-id-type="publisher-id">Front. Cell Dev. Biol.</journal-id><journal-title-group><journal-title>Frontiers in Cell and Developmental Biology</journal-title></journal-title-group><issn pub-type="epub">2296-634X</issn><publisher><publisher-name>Frontiers Media S.A.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">32083074</article-id><article-id pub-id-type="pmc">7005724</article-id><article-id pub-id-type="doi">10.3389/fcell.2019.00375</article-id><article-categories><subj-group subj-group-type="heading"><subject>Cell and Developmental Biology</subject><subj-group><subject>Original Research</subject></subj-group></subj-group></article-categories><title-group><article-title>ERas Enhances Resistance to Cisplatin-Induced Apoptosis by Suppressing Autophagy in Gastric Cancer Cell</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Tian</surname><given-names>Huajian</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Wenjun</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Meng</surname><given-names>Xiao</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Miaomiao</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Tan</surname><given-names>Junyang</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Jia</surname><given-names>Wenjuan</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Peining</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/87778/overview"></uri></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Jianshuang</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="c001"><sup>*</sup></xref><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/796728/overview"></uri></contrib><contrib contrib-type="author"><name><surname>Zhou</surname><given-names>Qinghua</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="c002"><sup>*</sup></xref><uri xlink:type="simple" xlink:href="http://loop.frontiersin.org/people/793992/overview"></uri></contrib></contrib-group><aff id="aff1"><sup>1</sup><institution>The First Affiliated Hospital, Biomedical Translational Research Institute, Jinan University</institution>,<addr-line>Guangzhou</addr-line>,<country>China</country></aff><aff id="aff2"><sup>2</sup><institution>Qingyuan People’s Hospital, The Sixth Affiliated Hospital of Guangzhou Medical University</institution>,<addr-line>Qingyuan</addr-line>,<country>China</country></aff><aff id="aff3"><sup>3</sup><institution>Department of Genetics, Yale School of Medicine, Yale University</institution>,<addr-line>New Haven, CT</addr-line>,<country>United States</country></aff><author-notes><fn fn-type="edited-by"><p>Edited by: Mark A. LaBarge, Irell & Manella Graduate School of Biological Sciences, United States</p></fn><fn fn-type="edited-by"><p>Reviewed by: Deyin Xing, Johns Hopkins University, United States; Dong-Joo (Ellen) Cheon, Albany Medical College, United States</p></fn><corresp id="c001">*Correspondence: Jianshuang Li, <email>lijianshuan1314@jnu.edu.cn</email></corresp><corresp id="c002">Qinghua Zhou, <email>gene@email.jnu.edu.cn</email></corresp><fn fn-type="other" id="fn004"><p>This article was submitted to Molecular Medicine, a section of the journal Frontiers in Cell and Developmental Biology</p></fn></author-notes><pub-date pub-type="epub"><day>21</day><month>1</month><year>2020</year></pub-date><pub-date pub-type="collection"><year>2019</year></pub-date><volume>7</volume><elocation-id>375</elocation-id><history><date date-type="received"><day>25</day><month>8</month><year>2019</year></date><date date-type="accepted"><day>16</day><month>12</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2020 Tian, Wang, Meng, Wang, Tan, Jia, Li, Li and Zhou.</copyright-statement><copyright-year>2020</copyright-year><copyright-holder>Tian, Wang, Meng, Wang, Tan, Jia, Li, Li and Zhou</copyright-holder><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p></license></permissions><abstract><p>Gastric cancer (GC), a common type of malignant cancer, remains the fifth most frequently diagnosed cancer and the third leading cause of cancer-related deaths worldwide. Despite developments in the treatment of GC, the prognosis remains poor. Embryonic stem cell-expressed Ras (ERas), a novel member of the Ras protein family, has recently been identified as an oncogene involved in the tumorigenic growth of embryonic stem cells. A recent study reported that ERas is expressed in most GC cell lines and GC specimens, and it promotes tumorigenicity in GC through induction of the epithelial mesenchymal transition (EMT) and activation of the PI3K/AKT pathway. Here, we found that ERas blocked autophagy flux in BGC-823 and AGS GC cells, which may occur through activation of the AKT/mTOR signaling pathway. Moreover, ERas overexpression suppressed cisplatin-induced apoptosis, and rapamycin treatment significantly attenuated ERas-mediated cisplatin resistance in GC cells. These data suggest that ERas may be a potential therapeutic target to improve the outcomes of GC patients by regulating the autophagy process.</p></abstract><kwd-group><kwd>gastric cancer</kwd><kwd>ERas</kwd><kwd>autophagy</kwd><kwd>apoptosis</kwd><kwd>resistance</kwd></kwd-group><counts><fig-count count="5"></fig-count><table-count count="0"></table-count><equation-count count="0"></equation-count><ref-count count="35"></ref-count><page-count count="8"></page-count><word-count count="0"></word-count></counts></article-meta></front></pmc><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Tian, Huajian" sort="Tian, Huajian" uniqKey="Tian H" first="Huajian" last="Tian">Huajian Tian</name></noRegion><name sortKey="Jia, Wenjuan" sort="Jia, Wenjuan" uniqKey="Jia W" first="Wenjuan" last="Jia">Wenjuan Jia</name><name sortKey="Li, Jianshuang" sort="Li, Jianshuang" uniqKey="Li J" first="Jianshuang" last="Li">Jianshuang Li</name><name sortKey="Meng, Xiao" sort="Meng, Xiao" uniqKey="Meng X" first="Xiao" last="Meng">Xiao Meng</name><name sortKey="Tan, Junyang" sort="Tan, Junyang" uniqKey="Tan J" first="Junyang" last="Tan">Junyang Tan</name><name sortKey="Wang, Miaomiao" sort="Wang, Miaomiao" uniqKey="Wang M" first="Miaomiao" last="Wang">Miaomiao Wang</name><name sortKey="Wang, Wenjun" sort="Wang, Wenjun" uniqKey="Wang W" first="Wenjun" last="Wang">Wenjun Wang</name><name sortKey="Zhou, Qinghua" sort="Zhou, Qinghua" uniqKey="Zhou Q" first="Qinghua" last="Zhou">Qinghua Zhou</name></country><country name="États-Unis"><noRegion><name sortKey="Li, Peining" sort="Li, Peining" uniqKey="Li P" first="Peining" last="Li">Peining Li</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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