摘要
目的:研究雌激素(E2)对人宫颈癌Hela细胞系增殖的影响及其与maspin基因蛋白表达的关系。方法:体外培养人宫颈癌HeLa细胞,MTT法测定不同E2水平的细胞生长曲线,流式细胞仪测定细胞周期及凋亡率,RT-PCR技术测定不同E2水平下maspin mRNA的表达变化。结果:MTT法及细胞流式技术均证实高浓度E2(10-6mol/l)可以明显促进宫颈癌Hela细胞的增殖和抑制其凋亡,其可促进细胞由G1期进入S期(P<0.05)。高E2水平组(10-6mol/l)细胞凋亡率明显弱于低E2水平组(P<0.05)。Maspin的阳性表达在高E2水平组(10-6mol/l)较低E2水平组(10-8mol/l)明显降低(P<0.05)。低E2水平组与对照组之间无明显差异(P>0.05)。结论:通过不同浓度组间比较,证实高浓度E2能明显增强宫颈癌Hela细胞的增殖及降低细胞的凋亡,且与maspin基因的表达成负相关,提示E2可能是通过减弱maspin基因的表达来发挥促进肿瘤生长的作用。
Objective: To research the effect of estradiol on proliferation of cervical cancer HeLa cells and its relationship with maspin gene expression. Methods: Human cervical cancer HeLa cells were cultured in vitro, MTT method was used tO detect cell growth curve of different levels of estradiol; flow cytometry was used to detect cell cycle and apoptotic rate, RT - PCR was used to detect the change of maspin mRNA expression of different levels of estradiol. Results: MTT method and flow cytometry confirmed that high concentration of es- tradiol (10-6mol/l) could promote the proliferation and inhibit the apoptosis of cervical cancer HeLa cells significantly, which could promote the cells from G1 phase into S phase (P 〈 0. 05 ) ; the apoptotic rate in high estradiol group ( 10 -6 moL/L) was statistically significantly lower than that in low estradiol group ( P 〈 0. 05 ) ; the positive expression rate of maspin in high estradiol group ( 10 -6 tool/L) was statistically significantly lower than that in low estradiol group (10-s mol/1 ) (P 〈 0. 05), but there was no statistically significant difference between low estradiol group and control group (P 〉 0. 05) . Conclusion : High concentration of estradiol can significantly promote the proliferation and inhibit the apoptosis of cervical cancer HeLa cells, which is negatively correlated with maspin gene expression, the result indicates that estradiol may play a promoting role in growth of cervical cancer by reducing maspin gene expression.
出处
《中国妇幼保健》
CAS
北大核心
2014年第11期1745-1747,共3页
Maternal and Child Health Care of China
基金
山东省自然科学基金资助项目〔ZR2012HL01〕