曲古抑菌素A对膀胱癌细胞的抑制作用及其机制  

Inhibitory effect of TSA on growth of bladder carcinoma cells and its mechanism

作　　者：李功成[1] 张旭[1] 李龙承[1] 叶章群[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院泌尿外科,湖北武汉430030

出　　处：《中国现代医学杂志》2005年第7期993-996,共4页China Journal of Modern Medicine

摘　　要：目的本研究探讨曲古抑菌素A(T SA)对人膀胱癌细胞的杀伤作用和机制。方法以不同浓度的T SA作用于体外培养的膀胱癌BIU-87细胞株;采用M TT法检测细胞生长抑制率;以流式细胞术(FC M)测定不同浓度的TSA作用前后膀胱癌细胞的凋亡情况及细胞周期变化;应用R T-PC R分析了TSA作用前后膀胱癌细胞中p21W m R N A表达的变化。结果TSA在纳摩尔级浓度即能有效抑制膀胱肿瘤细胞增殖,FC M AF1结果表明T SA能显著诱导细胞发生凋亡且主要诱导G1期细胞发生凋亡而出现凋亡峰,R T-PC R结果示T SA处理能显著诱导p21W m R N A表达。上述结果都呈现出明显的量-效与时-效关系。结论TSA在体AF1外能有效抑制对传统化疗耐药的人膀胱癌细胞生长,其抗肿瘤生长机制之一可能是通过上调p21W蛋白水平AF1实现的。This study was designed to investigate whether trichostatin A (TSA) possesses antitumor activity against Human bladder cancer cell and if any, its mechanism. Human bladder cancer BIU-87 cell lines was treated with different concentrations of TSA for different periods of time. After treatment, cell growth was measured by MTT assay. Cell apoptosis and changes in cell cycle were examined by means of flow cytometry (FCM). p21WAF1 mRNA expression was assessed by RT-PCR. TSA inhibited the proliferation of bladder cancer cell lines significantly at nanomolar concentrations in a time-and dose-dependent fashion, TSA treatment caused cell cycle arrest at G1 phase as shown by FCM and induced p21WAF1 mRNA expression. [Conclusion] TSA is able to inhibit bladder cancer cell lines growth in vitro, most likely through induction of p21WAF1 expression and subsequent arrest of cell cycling at G1 phase.

关 键 词：膀胱癌 组蛋白去乙酰化酶抑制剂 TSA P21^WAF1 

分 类 号：R969[医药卫生—药理学]