TY - JOUR
T1 - Trnalys-derived fragment alleviates cisplatin-induced apoptosis in prostate cancer cells
AU - Yang, Changwon
AU - Lee, Minkyeong
AU - Song, Gwonhwa
AU - Lim, Whasun
N1 - Funding Information:
This work was supported by the National Research Foundation of Korea grant funded Funding: This work was supported by the National Research Foundation of Korea grant funded by by the Ministry of Science and ICT, South Korea (grant number: 2018R1C1B6009048). the Ministry of Science and ICT, South Korea (grant number: 2018R1C1B6009048).
PY - 2021/1
Y1 - 2021/1
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Cisplatin
KW - GADD45A
KW - Prostate cancer
KW - TRNA-derived fragments
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U2 - 10.3390/pharmaceutics13010055
DO - 10.3390/pharmaceutics13010055
M3 - Article
AN - SCOPUS:85099182274
VL - 13
SP - 1
EP - 16
JO - Pharmaceutics
JF - Pharmaceutics
SN - 1999-4923
IS - 1
M1 - 55
ER -