EphA2 inhibits SRA01/04 cells apoptosis by suppressing autophagy via activating PI3K/Akt/mTOR pathway.

This study attempted to determine the effect of EphA2 on HO-treated lens epithelial cells (SRA01/04) and the underlying mechanisms. MTT assay and flow cytometry were performed to assess cell viability and cell apoptosis. Western blot was carried out to examine the levels of proteins associated with apoptosis and autophagy. Our results revealed that EphA2 significantly elevated the reduced cell viability, and inhibited the increased cell apoptosis in HO-treated SRA01/04 cells, along with the significant up-regulated Bcl-2 and down-regulated Cleaved-caspase-3 and Bax protein levels, but which were all abolished by Rapa (autophagy activator). We also found that EphA2 significantly suppressed cell autophagy in HO-treated SRA01/04 cells. Additionally, EphA2 significantly up-regulated the protein levels of p-Akt and p-mTOR in HO-treated SRA01/04 cells, and the inhibition of Akt by MK-2206 and inhibition of mTOR by Rapa both obviously reversed EphA2-mediated the inhibition of autophagy in HO-treated SRA01/04 cells. In summary, these data demonstrated that EphA2 inhibited the apoptosis of SRA01/04 cells by inhibiting autophagy via activating PI3K/Akt/mTOR pathway.