| Abstrakt: |
Backgrounds: Epidermal growth factor receptor kinase substrate 8-like 3 (EPS8L3) functions as a substrate of EGFR, and regulates signalings involved in cell proliferation, differentiation, and migration. The oncogenic role of EPS8L3 in distinct tumors was widely investigated, while the effect of EPS8L3 on gastric cancer (GC) remains unknown. Objectives: To investigate the effect of EPS8L3 on gastric cancer (GC). Results: EPS8L3 was elevated in GC tissues and cells, and predicted poor prognosis in the patients. Over-expression of EPS8L3 increased cell viability and reduced apoptosis of GC. However, cell viability of GC was decreased and the apoptosis was promoted by silence of EPS8L3. Knockdown of EPS8L3 down-regulated protein expression of p62, while up-regulated Beclin1 and LC3-II/LC3-I in GC cells. Phosphorylation of PI3K, AKT, and mTOR in GC cells was inhibited by EPS8L3 silence. Conclusion: EPS8L3 functioned as an oncogene in GC through suppression of cell apoptosis and autophagy via activation of PI3K/AKT/mTOR signaling. [ABSTRACT FROM AUTHOR] |
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