Ch1A-F enhanced sestrin 2 stability by inhibiting microRNA (miR)-27a-mediated degradation of sestrin 2 mRNA, which resulted in the increased expression of sestrin 2 protein, activation of the autophagy pathway, and inhibition of anchorage-independent growth of bladder cancer cell lines, including RT4, T24T, and UMUC3 cells [77]. Here, SESN2 is linked to urinary bladder cancer.