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目的探讨全反式维甲酸(ATRA)诱导食管癌EC9706细胞凋亡的作用及其机制。方法用不同浓度的ATRA处理EC9706细胞,采用四甲基偶氮唑盐(MTT)法检测ATRA对EC9706细胞的增殖抑制效应;采用流式细胞仪和原位末端标记(TUNEL)法检测细胞周期的变化和凋亡率;采用免疫组化S-P法,检测凋亡相关基因caspase-3和bcl-2的蛋白表达,并用病理图像分析软件进行半定量分析。结果ATRA对EC9706细胞有增殖抑制和诱导凋亡的作用;流式细胞仪检测显示,在G1期之前可出现Sub-G1峰,凋亡率最高为(32.6±0.4)%,并有浓度和时间依赖性;TUNEL法显示凋亡小体形成;EC9706细胞在凋亡过程中,凋亡相关基因caspase-3的蛋白表达增强,bcl-2的蛋白表达减弱。结论ATRA作用于食管癌EC9706细胞后将引起细胞凋亡的增加,这主要与ATRA能促进caspase-3的活化,并下调bcl-2的蛋白表达有关。
Objective To investigate the effect of all-trans retinoic acid (ATRA) on esophageal carcinoma EC9706 cell apoptosis and its mechanism. Methods EC9706 cells were treated with different concentrations of ATRA. The proliferation of EC9706 cells was detected by MTT assay. The cell cycle The protein expression of apoptosis-related genes caspase-3 and bcl-2 were detected by immunohistochemical SP method and semi-quantitative analysis was performed with pathological image analysis software. Results ATRA could inhibit proliferation and induce apoptosis of EC9706 cells. Flow cytometry showed that Sub-G1 peak appeared before G1 phase, with the highest apoptosis rate (32.6 ± 0.4)%, with concentration and time Dependent. TUNEL assay showed that apoptotic bodies were formed. In the process of apoptosis, EC9706 cells enhanced the expression of caspase-3 and decreased the expression of bcl-2 protein. CONCLUSION: ATRA can induce the apoptosis of esophageal carcinoma EC9706 cells, which is related to the fact that ATRA can promote the activation of caspase-3 and down-regulate the protein expression of bcl-2.