Ellagic acid induces apoptosis and autophagy in colon cancer through the AMPK/mTOR pathway

Ellagic acid (EA), found in fruits and foods, has been shown to be effective in the treatment of breast, colon and bladder cancer. However, due to the complexity of colon cancer, the therapeutic mechanism of EA for colon cancer is still unclear. Cell Counting Kit-8 (CCK-8) assay were employed to investigate the cell proliferation. Western blotting and flow cytometry assays were utilized to investigate apoptosis and autophagy in CRC cells (HCT116), respectively. Moreover, western blotting and luciferase reporter assays were evaluated the effect of EA on AMPK/mTOR pathway. Through flow cytometry analysis, EA could promote the apoptosis of HCT116 cells. In addition, EA can reduce the phosphorylation of mTOR, promoted phosphorylation of AMPK, and induced autophagy in HCT116 cells. Also, Dorsomorphin pretreatment can reduce the expression of autophagy protein, which indicates that EA induces autophagy through AMPK/mTOR pathway. These results suggest that EA in-hibits the growth of colon cancer through AMPK/mTOR pathway and induces apoptosis and protective autophagy.

Automated summary

Research has shown that ellagic acid (EA), found in fruits and foods, is effective in treating breast, colon, and bladder cancer. However, the therapeutic mechanism of EA for colon cancer is still unclear due to its complexity. In this study, cell counting, Western blotting, flow cytometry, and luciferase reporter assays were used to investigate the effects of EA on colon cancer cells (HCT116). The results revealed that EA promotes apoptosis, induces autophagy, and inhibits the growth of colon cancer through the AMPK/mTOR pathway.