Up-regulation of Bfl-1/A1 via NF-κB activation in cisplatin-resistant human bladder cancer cell line

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Up-regulation of Bfl-1/A1 via NF-κB activation in cisplatin-resistant human bladder cancer cell line
Jin Koo Kim; Kwang Dong Kim; E S Lee; Jong-Seok Lim; Hee Jun Cho; Hyun Kyung Yoon; Mi Young Cho; Kyoung Eun Baek; Yuk-Pheel Park; S G Paik; Yong Kyung Choe; Hee Gu Lee
Bibliographic Citation
Cancer Letters, vol. 212, no. 1, pp. 61-70
Publication Year
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.
Bfl-1, Bcl-2-related gene expressed in fetal liverBfl-1/A1cisplatin, cis-diamminedichloroplatinum (II)cisplatin-resistant bladder cancerdifferential displayNF-κB
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Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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