基础医学与临床 ›› 2022, Vol. 42 ›› Issue (1): 114-119.

• 研究论文 • 上一篇    下一篇

丙泊酚抑制人子宫内膜癌细胞系RL95-2增殖

李勇晓,孙燕,张瑞生   

  1. 郑州市妇幼保健院
  • 收稿日期:2020-11-16 修回日期:2021-05-10 出版日期:2022-01-05 发布日期:2022-01-05
  • 通讯作者: 李勇晓 E-mail:eta332@163.com
  • 基金资助:
    河南省医学科技攻关计划项目

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

  • Received:2020-11-16 Revised:2021-05-10 Online:2022-01-05 Published:2022-01-05

摘要: 目的:探究丙泊酚对子宫内膜癌细胞增殖凋亡的影响,以及对mTOR/S6K1信号通路的作用。方法:将人子宫内膜癌RL95-2细胞分为对照组和丙泊酚组,对照组不加干预,丙泊酚组加入不同浓度的丙泊酚对细胞进行干预。CCK-8法检测细胞增殖情况;克隆形成实验检测细胞克隆形成能力;流式细胞术测定细胞凋亡情况;比色法测定细胞半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3、Caspase-9活性;蛋白质免疫印迹法(WB)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)活化水平。结果:与对照组相比,丙泊酚各组RL95-2细胞增值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Akt、mTOR和S6K1蛋白活化水平显著降低(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的增殖、促进癌细胞凋亡。

Abstract: Objective: To investigate the influence of propofol on the proliferation and apoptosis of endometrial cancer cells and the effect on mTOR/S6K1 signaling pathway. Methods: Human endometrial cancer cell line RL95-2 was divided into control group and propofol group. The control group was not intervened, and the propofol group was intervened with different concentrations of propofol. 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; colorimetry was used to measure the activities of Caspase-3 and caspase-9; Western blot (WB) was used to detect the activation levels of protein kinase B (Akt), mammalian target of rapamycin (mTOR) and ribosomal protein S6 kinase 1 (S6K1). Results: Compared with those in 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 activation levels of Akt, mTOR and S6K1 were significantly lower (P < 0.05). Conclusion: Propofol may inhibit the proliferation and promote the apoptosis of endometrial cancer cells by regulating mTOR/S6K1 pathway.