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Up-regulation of Bfl-1/A1 via NF-κB activation in cisplatin-resistant human bladder cancer cell lineKim, Jin Koo; Kim, Kwang Dong; Lee, Eunsik; Lim, Jong-Seok; Cho, Hee-Jun; Yoon, Hyun Kyung; Cho, Mi-Young; Baek, Kyoung-Eun; Park, Yuk Pheel; Paik, Sang-Gi; Choe, Yong-Kyung; Lee, Hee Gu
Cancer letters, 08/2004, Letnik: 212, Številka: 1Journal Article
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 γ-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-κB) by cisplatin and γ-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-α-induced apoptosis in BOSC23 cells. Our findings suggest that the induction of Bfl-1/A1 by NF-κB may be important in controlling resistance to cisplatin responses in bladder tumor cells.
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