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作 者:郑景珍[1] 曹立赢[1] 王明君[1] 费乐学[1] 高建超[1] 陈磊[1] 戴世龙[1] 李浩[1] 张青松[1]
出 处:《贵州医药》2017年第4期348-350,共3页Guizhou Medical Journal
基 金:唐山市科技支撑项目(编号:14130260B)
摘 要:目的探讨TFⅢB亚单位Bdp1在5-甲基硫代腺苷(methylthioadenosine,MTA)对结肠癌RKO细胞增殖的抑制过程中的作用。方法采用Realtime PCR方法分析TFⅢB亚单位Bdp1基因mRNA水平的变化的转录水平;采用Western Blot方法分析TFⅢB亚单位Bdp1蛋白水平的变化;采用转染及荧光素酶报告基因的检测方法检测Bdp1基因荧光素酶活性。结果 MTA对结肠癌RKO细胞增殖抑制过程中,TFⅢB亚单位Bdp1在mRNA水平(0.441±0.03,P=0.001)和蛋白水平出现了明显的下调,同时报告基因Bdp1基因荧光素酶活性也出现了明显的下调(0.460±0.08,P=0.001)。结论 MTA对结肠癌RKO细胞增殖抑制过程中,TFⅢB亚单位Bdp1蛋白的下调可能起到重要作用。Objective To study the role of the Bdpl subunit of TFIIIB in the course of methylthioadenosine inhib- iting cell proliferation of colon cancer RKO cells. Methods The mRNA level of the subunits of Bdpl transcription was detected with method of Real time PCR, the level of Bdpl protein was detected with the method of western Blot (WB). The luciferase activity of Bdpl was detected with the method of luciferase reporter gene. Results The mRNA and protein level of the Bdpl were downregulated significantly (mRNA level : 0.441±0.03, P = 0. 001 ). The luciferase activity of Bdplwas downregulated significantly (0. 460±0.08, P= 0. 001 )in the above course. There were sta- tistical significantly differences (P〈0.05). Conclusion The subunit of the TFIIIB Bdpl might play a major role in the course of methylthioadenosine inhibiting cell proliferation of colon cancer RKO cells.
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