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Korean J Urol Oncol > Volume 1(2); 2003 > Article
The Korean Journal of Urological Oncology 2003;1(2): 186-192.
Establishment and Characterization of Cisplatin-Resistant Human Bladder Cancer Cells
Eunsik Lee 1, Cheol Kwak 1, Seok-Soo Byun 1, Dae Jung Lim 1, Jeong Hyun Kim 2,
Department of Urology, 1Seoul National University College of Medicine and 2the University of Ulsan College of Medicine, Seoul, Korea
Published online: June 30, 2003.
This study was designed to develop new cisplatin-resistant bladder tumor cell lines and to elucidate the underlying mechanism of acquired resistance to cisplatin. We have established 2 cisplatin-resistant cell lines, T24R1 and T24R2, from the T24 human bladder transitional carcinoma cell line, by continuous exposure to increasing concentrations of cisplatin. To elucidate the mechanisms of cisplatin resistance in these sublines, we investigated cellular morphology by light microscopy, growth rate, cell cycle by flow cytometry, glutathione(GSH) content, glutathione peroxidase(GP) and glutathione S-transferase(GST) activities, GST isoenzymes, P-glycoprotein expression, and the activity of topoisomerases I and II. The cytoplasms of the T24R1 and T24R2 cells displayed many vesicles and contained abundant granular material compared with the parent cells. Cell growth, DNA synthesis, and cell-cycle distribution of the cisplatin-resistant sublines did not differ from those of the parental T24 cells. T24R1 and T24R2 were 12.8-and 18-fold more resistant to cisplatin, respectively, than the parent cells were. GSH content, and GP and GST activities were elevated in the T24R2 cells compared with the T24 cells(p<0.05). Western blot analysis revealed that the expression of the GST-Ր isoenzyme was elevated in T24R2 cells. The sublines showed no induction of P-glycoprotein or topoisomerases I or II. In conclusion, an elevation in GSH metabolism and in the expression of the related enzymes appears to play an important role in the mechanism underlying cisplatin resistance in the T24R2 subline. (Korean J Uro-Oncol 2003;1:186-192)
Key Words: Bladder neoplasm; Cisplatin; Drug resistance
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