【摘要】 目的:探讨全反式维甲酸(all-tran retinoid acid,ATRA)对人食管鳞癌EC1细胞增殖、细胞周期和细胞凋亡的影响,并初步探讨其可能的机制。方法:分别以1、10和20μmol/L ATRA处理EC1细胞,应用MTT法检测细胞的增殖情况,FCM法检测细胞周期和细胞的早期凋亡,免疫细胞化学染色和蛋白质印迹法检测EC1细胞中p21和Bcl-2蛋白的表达。结果:与未经ATRA处理的对照组比较,1、10和20μmol/L ATRA可抑制EC1细胞的增殖,且呈剂量和时间依赖效应(P<0.05)。1、10和20μmol/L ATRA处理EC1细胞后,G0/G1期细胞比例[(66.58±0.30)%、(67.96±0.77)%和(75.11±2.24)%]高于对照组[(59.90±0.82)%](P<0.05),且细胞的早期凋亡率[(4.86±0.04)%、(7.35±0.04)%和(12.03±0.12)%]也高于对照组[(3.17±0.05)%](P<0.05)。ATRA作用后,EC1细胞中p21蛋白的表达水平上调,而Bcl-2蛋白的表达水平下调。结论:ATRA可以有效抑制食管鳞癌EC1细胞的增殖、阻滞细胞周期并诱导细胞凋亡,这个过程可能与p21表达上调和Bcl-2表达下调有关。更多还原

【Abstract】 Objective: To investigate the effects of ATRA (all-trans retinoic acid) on cell proliferation,cell cycle and apoptosis of human esophageal squamous cancer EC1 cells,and to explore its possible mechanism.Methods: The abilities of cellular proliferation of EC1 cells after treatment with 1,10 and 20 μmol/L ATRA were detected by MTT assay,and the cell cycle distribution and the apoptosis of EC1 cells were determined by flow cytometry.The expressions of p21 and Bcl-2 in EC1 cells after treatment with 1,10 and 20 μmol/L ATRA were detected by immunocytochemistry and Western blotting.Results: As compared with the EC1 cells without treatment (as a control),the proliferation of EC1 cells was inhibited by ATRA in a dose- and time-dependent manner (P < 0.05).The proportions of G 0 and G 1 cells were higher in EC1 cells after treatment with 1,10 and 20 μmol/L ATRA than that of the control cells (66.58± 0.30)%,(67.96±0.77)% and (75.11±2.24)% vs (59.90±0.82)%,P < 0.05.The apoptotic rates of EC1 cells treated with 1,10 and 20 μmol/L ATRA were higher than that of the control cells (4.86±0.04)%,(7.35± 0.04)% and (12.03±0.12)% vs (3.17±0.05)%,P < 0.05.The expression level of p21 in EC1 cells treated with ATRA was up-regulated,but the expression level of Bcl-2 was down-regulated.Conclusion: ATRAcan inhibit the proliferation of human esophageal squamous cancer EC1 cells and induce G 0 /G 1 phase blocking and cell apoptosis.This effect may be related with the up-regulation of p21 expression and down-regulation of Bcl-2 expression.更多还原