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目的探讨吡柔比星对膀胱癌细胞增殖的影响及其作用机制。方法膀胱癌细胞T24和BIU-87分别用0.4、0.8、1.6、3.2mg/L的吡柔比星处理24、48、72h,用四甲基偶氮唑盐(MTT)检测细胞增殖,流式细胞术检测细胞凋亡率,qRT-PCR、RT-PCR检测磷脂酶Cε(PLCε)mRNA及凋亡调控基因Bcl-2mRNA的表达,蛋白质印迹法检测PLCε蛋白的表达。将膀胱癌细胞分为空白组、吡柔比星处理组、Ad-shPLCε处理组、吡柔比星联合PLCε干扰腺病毒载体(Ad-shPLCε)处理组,检测并比较各组细胞增殖和Bcl-2蛋白的表达量。结果在膀胱癌细胞T24、BIU-87中,吡柔比星对细胞的抑制率呈浓度、时间依赖性,即随着药物浓度增加、处理时间延长,细胞抑制率升高;吡柔比星促进T24和BIU-87细胞凋亡,并且抑制PLCε和Bcl-2表达。吡柔比星处理组、Ad-shPLCε处理组、Ad-shPLCε联合吡柔比星处理组均能抑制细胞增殖和Bcl-2表达,且Ad-shPLCε联合吡柔比星处理组的抑制作用高于吡柔比星处理组,差异有统计学意义(P<0.05)。结论吡柔比星能有效抑制膀胱癌细胞的增殖,可能与其抑制PLCε癌基因及下游Bcl-2基因的表达有关。
Objective To investigate the effect of pirarubicin on the proliferation of bladder cancer cells and its mechanism. Methods Bladder cancer cells T24 and BIU-87 were treated with 0.4, 0.8, 1.6 and 3.2 mg / L of pirarubicin for 24, 48, and 72 h, respectively. Cell proliferation was measured by MTT, Cell apoptosis rate was detected by qRT-PCR. The expression of PLCε mRNA and Bcl-2 mRNA were detected by RT-PCR. The expression of PLCε protein was detected by Western blotting. The bladder cancer cells were divided into blank group, pirarubicin treatment group, Ad-shPLCε treatment group, pirarubicin and PLCε interference adenovirus vector (Ad-shPLCε) treatment group, detection and comparison of cell proliferation and Bcl- 2 protein expression level. Results The inhibitory rate of pirarubicin on bladder cancer cells T24 and BIU-87 was concentration-dependent and time-dependent, that is, as the drug concentration was increased, the treatment time was prolonged and the cell inhibition rate was increased. Pirarubicin promoted T24 and BIU-87 cells and inhibited PLC [epsilon] and Bcl-2 expression. Pirarubicin treatment, Ad-shPLCε treatment and Ad-shPLCε combined with pirarubicin could inhibit cell proliferation and Bcl-2 expression, and the inhibitory effect of Ad-shPLCε combined with pirarubicin treatment group was higher than Pirarubicin treatment group, the difference was statistically significant (P <0.05). Conclusion Pirarubicin can effectively inhibit the proliferation of bladder cancer cells, which may be related to its inhibition of PLCε oncogene and downstream Bcl-2 gene expression.