Mechanism of cisplatin resistance in human urothelial carcinoma cells

被引:15
作者
Yu, Hui-Min [2 ]
Wang, Tsing-Cheng [1 ]
机构
[1] Acad Sinica, Inst Cellular & Organism Biol, Taipei 115, Taiwan
[2] Natl Def Med Ctr, Grad Inst Life Sci, Taipei 114, Taiwan
关键词
Urothelial carcinoma; Cisplatin; Bcl-2; HO-1; p16; BLADDER-CANCER CELLS; CELLULAR ACCUMULATION; HEME OXYGENASE-1; DOWN-REGULATION; INDUCED APOPTOSIS; ACQUIRED-RESISTANCE; HIGH CYTOTOXICITY; DRUG-RESISTANCE; PROXIMAL TUBULE; OVARIAN-CANCER;
D O I
10.1016/j.fct.2012.01.040
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
An isogenic pair of cisplatin-susceptible (NTUB1) and -resistant (NTUB1/P) human urothelial carcinoma cell lines was used to elucidate the mechanism of cisplatin resistance. The significantly lower intracellular platinum (IP) concentration, which resulted from the decreased cisplatin uptake, was found in NTUB1/P cells. The enhancement of IP concentration did not increase the susceptibility of NTUB1/P cells to cisplatin treatment. The reduction of IP concentration as well was unable to enhance the cisplatin-resistance in susceptible NTUB1 cells. This indicated that reduction of IF concentration was not the account for the development of cisplatin resistance here. Instead, the over expression of anti-apoptotic Bcl-2, anti-oxidative heme oxygenase-1 (HO-1) and cell cycle regulator p16INK4 seemed to be more important for the gaining of cisplatin in these human urothelial carcinoma cell. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1226 / 1237
页数:12
相关论文
共 89 条
[1]   MUTUAL DEPENDENCE OF NA,K-ATPASE ALPHA-SUBUNITS AND BETA-SUBUNITS FOR CORRECT POSTTRANSLATIONAL PROCESSING AND INTRACELLULAR-TRANSPORT [J].
ACKERMANN, U ;
GEERING, K .
FEBS LETTERS, 1990, 269 (01) :105-108
[2]   Cisplatin sensitivity of oral squamous carcinoma cells is regulated by Na+,K+-ATPase activity rather than copper-transporting P-type ATPases, ATP7A and ATP7B [J].
Ahmed, Zunaid ;
Deyama, Yoshiaki ;
Yoshimura, Yoshitaka ;
Suzuki, Kuniaki .
CANCER CHEMOTHERAPY AND PHARMACOLOGY, 2009, 63 (04) :643-650
[3]   The tumor suppressor p16INK4a gene is a regulator of apoptosis induced by ultraviolet light and cisplatin [J].
Al-Mohanna, MA ;
Manogaran, PS ;
Al-Mukhalafi, Z ;
Al-Hussein, KA ;
Aboussekhra, A .
ONCOGENE, 2004, 23 (01) :201-212
[4]  
ANDREWS PA, 1991, CANCER RES, V51, P3677
[5]  
ANDREWS PA, 1987, CANCER CHEMOTH PHARM, V19, P149
[6]   New roles for an old enzyme: Na,K-ATPase emerges as an interesting drug target [J].
Aperia, A. .
JOURNAL OF INTERNAL MEDICINE, 2007, 261 (01) :44-52
[7]   C-myc down-regulation increases susceptibility to cisplatin through reactive oxygen species-mediated apoptosis in M14 human melanoma cells [J].
Biroccio, A ;
Benassi, B ;
Amodei, S ;
Gabellini, C ;
Del Bufalo, D ;
Zupi, G .
MOLECULAR PHARMACOLOGY, 2001, 60 (01) :174-182
[8]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[9]   The relationship between cisplatin-induced reactive oxygen species, glutathione, and BCL-2 and resistance to cisplatin [J].
Brozovic, Anamaria ;
Ambriovic-Ristov, Andreja ;
Osmak, Maja .
CRITICAL REVIEWS IN TOXICOLOGY, 2010, 40 (04) :347-359
[10]  
Bureau of Health Promotion Executive Yuan Taiwan ROC, 2005, CANC REG ANN REP 200