去甲斑蝥素干预Wnt/β-catenin信号通路诱导人卵巢癌SKOV3细胞凋亡
Norcantharidin induces apoptosis through Wnt/β-catenin signaling pathway in human ovarian cancer SKOV3 cells
赵月渟 1王英 2郜梦婷 1董秀2
作者信息
- 1. 辽宁中医药大学研究生学院,辽宁 沈阳 110847
- 2. 辽宁中医药大学中西医结合学院,辽宁 沈阳 110847
- 折叠
摘要
目的:讨论去甲斑蝥素对人卵巢癌SKOV3细胞凋亡的影响,并探讨其作用机制.方法:体外培养人卵巢癌SKOV3细胞,将浓度为52 μmol/L去甲斑蝥素作用于人卵巢癌SKOV3细胞后,将卵巢癌SKOV3细胞分为对照组、去甲斑蝥素组(52 μmol/L),等待卵巢癌细胞贴壁药物作用6 h后,在倒置显微镜下观察卵巢癌SKOV3细胞的形态学变化,荧光显微镜观察细胞核的变化;药物作用24 h后,采用流式细胞术检测线粒体膜电位的变化情况,采用Western blot法检测药物作用后对卵巢癌SKOV3细胞凋亡相关蛋白Bax、Bcl-2以及Wnt/β-catenin信号通路相关蛋白β-catenin表达水平的影响.结果:与对照组比较,去甲斑蝥素抑制卵巢癌SKOV3细胞增殖,降低线粒体膜电位,诱导人卵巢癌SKOV3细胞凋亡,升高Bax的表达水平,抑制Bcl-2蛋白表达水平,降低Wnt/β-catenin信号通路相关蛋白β-catenin的表达水平.结论:去甲斑蝥素诱导卵巢癌SKOV3细胞凋亡的机制可能与调控Wnt/β-catenin信号通路相关.
Abstract
Objective:To investigate the effect of Norcantharidin(NCTD)on the apoptosis of human ovarian cancer SKOV3 cells and its mechanism.Methods:Human ovarian cancer SKOV3 cells were cultured in vitro and treated with 52 μmol/L NCTD.The SKOV3 cells were divided into the control group and NCTD group(52 μmol/L).The morphological changes of SKOV3 cells were observed under an inverted microscope,and the changes of nucleus were observed under a fluorescence microscope.The changes of mitochondrial membrane potential were detected by flow cytometry after drug treatment for 24 h.Western blot was used to detect the expression levels of apoptosis-related proteins Bax,Bcl-2 and Wnt/β-catenin signaling pathway-related protein β-catenin in SKOV3 cells after drug treatment for 24 h.Result:Compared with that in the control group,NCTD inhibited the proliferation of SKOV3 cells,reduced mitochondrial membrane potential,induced apoptosis of SKOV3 cells,increased the expression of Bax protein,decreased the expression of Bcl-2 protein and β-catenin.Conclusion:NCTD-induced apoptosis of ovarian cancer SKOV3 cells may be related to the regulation of Wnt/β-catenin signaling pathway.
关键词
去甲斑蝥素/凋亡/卵巢癌SKOV3细胞/Wnt/β-catenin信号通路Key words
norcantharidin/apoptosis/ovarian cancer SKOV3 cell/Wnt/β-catenin signaling pathway引用本文复制引用
基金项目
辽宁省教育厅重点攻关项目(L202069)
出版年
2024
国家科技期刊平台
NSTL
万方数据