曲古抑菌素A对肺癌细胞株H322抑制效应及机制的研究

摘要

Objective To assess the growth-inhibiting effects of trichostatin A (TSA)on human lung cancer cell strains H322 and its mechanism in vitro. Methods H322 cells were exposed to TSA at different concentration,then the growth inhibiting effects of the cell line were detected with MTT assay ;The change of the cell cycle and apoptosis was analyzed with flow cytometry. Protein p21, survivin and ERK expression were detected by Western blot Results TSA exposure caused inhibition effects on H322 cells in a dose and time- dependent manner;The proportion of apoptosis,G2/M phase increased after exposed to TSA;In addition,the expression of cell cycle molecule p21 was upgraded,and apoptosis molecule survivin and signaling molecule pERK were depleted after H322 cells treated with TSA. Conclusions TSA exhibits significant antitumor activity against human lung cancer cell strains H322 by inducing the cell cycle arrest and apoptosis.This may be caused by upgrading of expression p21 and downgrading of survivin and pERK.%目的 评价曲古抑菌素A(TSA)对肺癌细胞株H322的生长抑制效应及机制.方法 以四氮甲基唑蓝、流式细胞术观察TSA作用后,肺癌细胞株H322的生长抑制情况以及细胞周期、细胞凋亡等变化,Western blot分析细胞周期相关蛋白p21、抗凋亡蛋白survivin及细胞外信号调节激酶(ERK)的表达.结果 TSA对H322具有时间依赖性和浓度依赖性的生长抑制作用；TSA作用48h及96h后,H322细胞凋亡及G2/M期细胞明显增加(P＜0.05).p21蛋白表达水平显著提高,survivin蛋白及磷酸化ERK蛋白表达显著下降.结论 TSA对肺癌细胞株H322生长具有抑制作用,其机制可能是上调p21蛋白的表达,引起细胞周期的阻滞；同时抑制survivin的表达,阻断ERK信号通路,导致细胞凋亡.