基础医学与临床 ›› 2022, Vol. 42 ›› Issue (1): 114-119.doi: 10.16352/j.issn.1001-6325.2022.01.015

• 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 麻醉科,河南 郑州 450000
  • 收稿日期:2020-11-16 修回日期:2021-05-18 出版日期:2022-01-05 发布日期:2022-01-05
  • 通讯作者: * 1113452319@qq.com
  • 基金资助:
    河南省医学科技攻关计划(201602135)

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

LI Yong-xiao*, SUN Yan, ZHANG Rui-sheng   

  1. Department of Anesthesiology, Zhengzhou Maternal and Child Health Hospital, Zhengzhou 450000, China
  • Received:2020-11-16 Revised:2021-05-18 Online:2022-01-05 Published:2022-01-05
  • Contact: * 1113452319@qq.com

摘要: 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。

关键词: 丙泊酚, 子宫内膜癌, mTOR信号通路, 增殖, 凋亡

Abstract: 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.

Key words: propofol, endometrial carcinoma, mTOR signaling pathway, proliferation, apoptosis

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