Cisplatin is a standard treatment for
prostate cancer, which is the third leading cause of
cancer-related deaths among men globally. However, patients who have undergone
cisplatin can rxperience relapse.
tRNA-derived fragments (tRFs) are small non-coding RNAs generated via
tRNA cleavage; their physiological activities are linked to the development of human diseases. Specific tRFs, including tRF-315 derived from
tRNALys, are highly expressed in
prostate cancer patients. However, whether tRF-315 regulates
prostate cancer cell proliferation or apoptosis is unclear. Herein, we confirmed that tRF-315 expression was higher in
prostate cancer cells (LNCaP, DU145, and PC3) than in normal prostate cells. tRF-315 prevented
cisplatin-induced apoptosis and alleviated
cisplatin-induced
mitochondrial dysfunction in LNCaP and DU145 cells. Moreover, transfection of tRF-315 inhibitor increased the expression of apoptotic pathway-related
proteins in LNCaP and DU145 cells. Furthermore, tRF-315 targeted the tumor suppressor gene GADD45A, thus regulating the cell cycle, which was altered by
cisplatin in LNCaP and DU145 cells. Thus, tRF-315 protects
prostate cancer cells from mitochondrion-dependent apoptosis induced by
cisplatin treatment.