tRNA(Lys)-Derived Fragment Alleviates Cisplatin-Induced Apoptosis in Prostate Cancer Cells
- Authors
- Yang, Changwon; Lee, Minkyeong; Song, Gwonhwa; Lim, Whasun
- Issue Date
- 1월-2021
- Publisher
- MDPI
- Keywords
- prostate cancer; tRNA-derived fragments; cisplatin; apoptosis; GADD45A
- Citation
- PHARMACEUTICS, v.13, no.1, pp.1 - 16
- Indexed
- SCIE
SCOPUS
- Journal Title
- PHARMACEUTICS
- Volume
- 13
- Number
- 1
- Start Page
- 1
- End Page
- 16
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/50266
- DOI
- 10.3390/pharmaceutics13010055
- ISSN
- 1999-4923
- Abstract
- 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 tRNA(Lys), 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.
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Collections - Graduate School > Department of Biotechnology > 1. Journal Articles
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