丙泊酚抑制人子宫内膜癌细胞系RL95-2增殖

Propofol inhibits proliferation of human endometrial cancer cell line RL95-2

目的探究丙泊酚对子宫内膜癌细胞系RL95-2增殖和凋亡的影响,以及对mTOR/S6K1信号通路的作用。方法将RL95-2细胞分为对照组和丙泊酚组(加入不同浓度的丙泊酚)。CCK-8法检测细胞增殖;克隆形成实验检测细胞克隆形成能力;流式细胞测量术检测细胞凋亡;比色法测定细胞caspase-3和caspase-9活性;蛋白质免疫印迹法(Western blot)检测细胞蛋白激酶B(Akt)、哺乳动物雷帕霉素靶蛋白(mTOR)和核糖体蛋白S6激酶1(S6K1)磷酸化水平。结果与对照组相比,丙泊酚各组RL95-2细胞增殖率和细胞克隆形成能力均显著降低(P<0.05),细胞凋亡率以及细胞caspase-3和caspase-9活性均显著升高(P<0.05),细胞p-Akt、p-mTOR和p-S6K1蛋白磷酸化水平显著降低(P<0.05)。结论丙泊酚可能通过调控mTOR/S6K1通路,抑制子宫内膜癌细胞系的增殖、促进癌细胞凋亡。

Objective To investigate the influence of propofol on the proliferation and apoptosis of endometrial cancer cell line RL95-2 and the effect on mTOR/S6K1 signaling pathway.Methods Human endometrial cancer cell line RL95-2 was divided into control group and propofol group(different concentrations of propofol were added).CCK-8 method was used to detect cell proliferation;Clone formation assay was used to detect the ability of cell clone formation;Flow cytometry was used to measure cell apoptosis;Colorimetric was used to measure the activities of caspase-3 and caspase-9;Western blot was used to detect the phosphorylation levels of protein kinase B(Akt),mammalian target of rapamycin(mTOR)and ribosomal protein S6 kinase 1(S6K1).Results Compared with the control group,the proliferation rate and colony forming ability of RL95-2 cells in propofol groups were significantly lower(P<0.05),the apoptosis rate and the activities of caspase-3 and caspase-9 were significantly higher(P<0.05),the phosphorylation levels of p-Akt,p-mTOR and p-S6K1 were significantly lower(P<0.05).Conclusions Propofol may inhibit the proliferation and promote the apoptosis of endometrial cancer cell line by regulating mTOR/S6K1 pathway.