论文部分内容阅读
目的 :探讨组蛋白去甲基化酶JMJD2B影响人结直肠癌细胞恶性表型所介导的信号通路。方法 :以RNA干扰技术靶向沉默人结直肠癌细胞HCT116和SW480中JMJD2B的表达,采用蛋白质印迹法检测人结直肠癌细胞ERK-MAPK信号通路的变化,并分别采用CCK-8、流式细胞分析检测细胞增殖和细胞周期分布、凋亡情况。结果:转染JMJD2B si RNA能特异性抑制JMJD2B的表达并导致ERK2表达下调,其磷酸化水平也降低,肿瘤细胞发生G2/M或G0/G1期阻滞,细胞凋亡比例增加,增殖显著受抑(P<0.05)。结论:抑制JMJD2B可通过阻断ERK-MAPK信号转导而抑制人结直肠癌细胞的恶性表型。
Objective: To investigate the signaling pathway mediated by histone demethylase JMJD2B in malignant phenotype of human colorectal cancer cells. METHODS: The expression of JMJD2B in human colorectal cancer cells HCT116 and SW480 was detected by RNA interference technique. The changes of ERK-MAPK signal pathway in human colorectal cancer cells were detected by Western blotting. The expression of ERK-MAPK signal pathway in human colorectal cancer cells was detected by flow cytometry Analysis of cell proliferation and cell cycle distribution, apoptosis. Results: Transfection of JMJD2B si RNA specifically inhibited the expression of JMJD2B and resulted in the down-regulation of ERK2 expression. The phosphorylation level of JMJD2B was also decreased. G2 / M or G0 / G1 arrest was observed in tumor cells, and the percentage of apoptosis was significantly increased (P <0.05). Conclusion: Inhibition of JMJD2B inhibits the malignant phenotype of human colorectal cancer cells by blocking ERK-MAPK signal transduction.