茶多酚诱导膀胱癌T24细胞株凋亡及上调PTEN表达

目的 探讨茶多酚抑制膀胱癌细胞生长的可能分子机制。方法 采用MTT法和流式细胞术,观察膀胱癌细胞系T24经不同浓度的茶多酚处理后对细胞生长以及PTEN蛋白表达的影响。结果茶多酚以剂量依赖的方式抑制膀胱癌细胞的生长,加入0、50、100、200、400μg/ml茶多酚的T24细胞抑制率分别为0%、11.2%、33.4%、36.9%、67.5%。流式细胞仪直方图上可见亚二倍体峰,癌细胞出现凋亡,凋亡率分别为6.8%、25.1%、28.6%、36.6%、41.1%;同时,随茶多酚作用浓度的增加,出现G1/S阻滞细胞逐渐增多,细胞分裂增殖指数（PI）降低;而细胞PTEN蛋白表达水平由（37.66±0.49）逐渐增加至（163.92±3.36）（P〈0.01）。结论 茶多酚对T24细胞生长具有抑制作用,其机制可能是通过上调PTEN蛋白表达影响细胞周期和诱导细胞凋亡。PTEN蛋白表达水平的上调可能具有逆转细胞恶性生物学行为作用。

Study on the tea polyphenol''''s effects of inducing apoptosis of bladder carcinoma cell T24 and up-regulating PTEN ''''s expression

Objective To explore the molecular mechanism of inhibition effect of tea polyphenols on the growth＂ of bladder carcinoma cell lines. Methods MTI＂ assay and flow cytometry（FCM） analysis were applied to investigate the effects of TP on the cellular growth, proliferation cycle, apoptosis, and the expression of PTEN in bladder carcinoma cell lines. Results To inhibited the growth and inducted apoptosis of T24 ceils in a dose - dependent manner, under the dosages of 0μg·ml^-1,50μg·ml^-1 , 100μg· ml^-1,200μg·ml^-1 and 400μg· ml^-1 average inhibitory rate were 0%, 11.2%, 33.4%, 36.9% and 67.5 %, and hypodiploid peaks on FCM histogram. Apoptosis rate were 6.8% ,25.1% ,28.6% ,36.6% ,41,1% ;Moreover, the cell cycle could be arrested at G1/S checkpoint, also made G1 phase cell markedly increasing and the cell proliferating index （P1） also decreased. At the same time, the expression of PTEN increased from 37.66 ± 0.49 to 163.92 ± 3.36（ P 〈 0.01） with TP treatment. Conclusion TP has the inhibitory effects on the cellular growth, and the mechanism may be associated with influence in the cell cycle and induction of apoptosis in T24 cell lines, The cell cycle and apoptosis are associated with TP - induced increase of PTEN protein level in the level cell lines. At the same time, the up - regulation of the PTEN ＇ s expression by TP also has a possible reversing effects on malignant tumor cells .