Up-regulation of Bfl-1/A1 via NF-kappa B activation in cisplatin-resistant human bladder cancer cell line
- Authors
- Lee, E; Kim, JK; Kim, KD; Lim, JS; Cho, HJ; Yoon, HK; Cho, MY; Baek, KE; Park, YP; Paik, SG; Choe, YK; Lee, HG
- Issue Date
- Aug-2004
- Publisher
- ELSEVIER IRELAND LTD
- Citation
- CANCER LETTERS, v.212, no.1, pp 61 - 70
- Pages
- 10
- Journal Title
- CANCER LETTERS
- Volume
- 212
- Number
- 1
- Start Page
- 61
- End Page
- 70
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/148917
- DOI
- 10.1016/j.canlet.2004.02.021
- ISSN
- 0304-3835
1872-7980
- Abstract
- The potent anti-cancer agent cis-diamminedichloroplatinum (II) (cisplatin) is currently used for treating bladder cancer. However, clinical use of this drug for long periods is often limited because of the appearance of cisplatin-resistant bladder tumor cells. We employed the method of a differential display reverse transcriptase polymerase chain reaction to identify the differentially expressed genes in the parental human bladder cancer cell line, T24 and three cisplatin-resistant cell lines. We report here that cisplatin-resistant cell lines overexpress Bcl-2 family protein Bcl-2-related gene expressed in fetal liver (Bfl-1)/A1 as compared with their parental cell. Cisplatin and gamma-irradiation induced expression of Bfl-1/A1 in T24R2 cells but not in T24 cells. Among Bcl-2 family members, Bfl-1/A1 showed the most significant alteration of the expression level in resistant cells. The nuclear translocation of nuclear factor-kappaB (NF-kappaB) by cisplatin and gamma-irradiation selectively occurred in T24R2 cells. Mitochondrial depolarization and cell death by cisplatin were also prevented in T24R2 cells. Moreover, Bfl-1/A1 inhibited cisplatin- and TNF-alpha-induced apoptosis in BOSC23 cells. Our findings suggest that the induction of Bfl-1/A1 by NF-kappaB may be important in controlling resistance to cisplatin
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