Interestingly, our results showed that the reduction in in cell viability, the increase in apoptosis, as well as the decrease in p-mTOR, p-p70s6K, and survivin expression elicited by sestrin 2 overexpression were attenuated or abrogated after AMPK inhibition with compound C. Thus, our findings indicate that sestrin 2 inhibits mTORC1 activity via AMPKα1, and down-regulates survivin expression in CRC cells. Here, SESN2 is linked to colorectal carcinoma.