雷公藤甲素对非小细胞肺癌细胞系A549增殖的抑制和凋亡的诱导

目的探讨雷公藤甲素(TP)通过调控趋化因子受体4(CXCR4)基因表达对人非小细胞肺癌(A549)细胞增殖和凋亡的影响。方法实验分为4组:对照组、TP组(100 nm/L TP处理细胞)、CXCR4+TP组(转染质粒及TP处理细胞)和NC+TP组(转染空载质粒及TP处理细胞)。RT-qPCR和Western blot检测CXCR4表达以及转染效果;MTT法检测细胞增殖;AnnexinⅤ-FITC/PI双染色法检测细胞凋亡;Western blot检测增殖及凋亡相关蛋白表达。结果雷公藤甲素能够抑制A549细胞中CXCR4 mRNA和蛋白的表达(P<0. 05)。雷公藤甲素可抑制A549细胞增殖,诱导其凋亡(P<0. 05)。转染pc DNA-CXCR4能够上调CXCR4 mRNA和蛋白的表达(P<0. 05)。上调CXCR4的表达能够部分逆转雷公藤甲素对A549细胞增殖抑制和凋亡诱导的作用(P<0. 05)。结论雷公藤甲素可能通过下调CXCR4的表达抑制A549细胞增殖,诱导细胞凋亡。

Triptolide inhibits the proliferation and promotes apoptosis of non-small cell lung cancer cell line A549

Objective To investigate the effect of triptolide( TP) on the proliferation and apoptosis of human nonsmall cell lung cancer cell A549 by regulating the expression of chemokine receptor 4( CXCR4) gene. Methods The experiment was divided into 4 groups: control group,TP group( 100 nm/L TP-treated cells),CXCR4 +TP group( transfected plasmid TP-treated cells) and NC+TP group( empty plasmid TP-treated cells). The expression of CXCR4 and transfection were detected by RT-qPCR and Western blot. Cell proliferation was detected by MTT assay,apoptosis was detected by Annexin V-FITC/PI double staining,proliferation and apoptosis-related protein expression were detected by Western blot. Results Triptolide inhibited the expression of CXCR4 mRNA and protein in A549 cells( P < 0. 05). Triptolide inhibited the proliferation of A549 cells and induced apoptosis( P<0. 05).Transfection of pcDNA-CXCR4 up-regulated the expression of CXCR4 mRNA and protein( P < 0. 05).Up-regulation of CXCR4 expression partially reversed the effect of triptolide on proliferation inhibition and apoptosis induction of A549 cells( P<0. 05). Conclusions Triptolide may inhibit the proliferation of non-small cell lung cancer A549 cells and induce apoptosis by down-regulating the expression of CXCR4.