4.7 Article

ERas Enhances Resistance to Cisplatin-Induced Apoptosis by Suppressing Autophagy in Gastric Cancer Cell

期刊

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2019.00375

关键词

gastric cancer; ERas; autophagy; apoptosis; resistance

资金

  1. National Natural Science Foundation of China [81601299, 81800833, 81802189]
  2. National Key R&D Program of China [2018YFC2002000]
  3. 111 Project [B16021]
  4. China Postdoctoral Science Foundation [2018M631054]
  5. Natural Science Foundation of Guangdong Province [2018A0303131002]

向作者/读者索取更多资源

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.

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