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Korean J Urol Oncol > Volume 9(2); 2011 > Article
The Korean Journal of Urological Oncology 2011;9(2): 62-67.
Cis-platin 내성 방광암세포주에 대한 Trichostatin A의 항암효과 분석
박지현1, 변석수1, 이정은1, 오종진1, 이상철1, 홍성규1, 윤철용1, 이은식2, 이상은1
1분당서울대학교병원 비뇨기과, 2서울대학교 의과대학 비뇨기과학교실
An Anticancer Effect of Trichostatin A in Cis-platin-resistant BladderCancer Cells
Jihyun Park 1, Seok-Soo Byun 1, Jeong Eun Lee 1, Jong Jin Oh 1, Sang Chul Lee 1, Sung Kyu Hong 1, Cheol Yong Yoon 1, Eunsik Lee 2, Sang Eun Lee 1
Department of Urology, 1Seoul National University Bundang Hospital, Seongnam, 2Seoul National University College of Medicine, Seoul, Korea
Published online: August 30, 2011.
To determine anti-tumor effect of a histone deacetylase(HDAC) inhibitor, trichostatin A(TSA) in cis-platin resistant human bladder cancer cells(T24R2).
Materials and Methods:
T24 bladder cancer cell line and T24R2 were exposed to escalating dose of TSA and tumor cell proliferation was examined by CCK-8 assay. To evaluate the changes in cell cycle and apoptosis, flow cytometry was used and clonogenic assay was performed. Expression of p21WAF1/CIP1, cIAP1, XIAP, Bcl-2, and Bax were analyzed by Western blot.
Acute TSA administration(0.1-2ՌM for 24-72hours) suppressed tumor cell proliferation in a time- and dose-dependent manner(p<0.05) in all two bladder tumor cell lines. TSA induced G1 phase cell cycle arrest in both bladder cell lines and higher-fraction of sub-G1(apoptotic portion) with 0.5ՌM in T24R2. A significant decrease in colony number was seen with the TSA treatment in the two cell lines. Western blot analysis revealed up-regulated p21 and bax, and down-regulated bcl-2, cIAP1 and xIAP with the increasing concentrations of TSA in both cell lines.
Our results suggest anti-tumor effect of TSA in inhibiting bladder cancer growths and its potential role as an agent for treating cisplatin-resistant bladder cancer. (Korean J Urol Oncol 2011;9:62-67)
Key Words: Urinary bladder neoplasms; Trichostatin A; Histone deacetylases
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