ERas Enhances Resistance to Cisplatin-Induced Apoptosis by Suppressing Autophagy in Gastric Cancer Cell
Identifieur interne : 000167 ( an2020/Analysis ); précédent : 000166; suivant : 000168ERas 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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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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