淫羊藿素在Wnt/β-catenin通路介导的乳腺癌细胞上皮间质化过程中的作用机制  

Mechanism of icariin on Wnt/β-catenin pathway mediated epithelial-mesenchymal transition in breast cancer cells

作　　者：亓新峰 亓晓 侯双霞 Qi Xinfeng;Qi Xiao;Hou Shuangxia(Department of Pharmacy,The Second Children&Women's Healthcare of Jinan City,Jinan 271100;Department of Internal Medicine,Yantai Hospital of Traditional Chinese Medicine,Yantai 264013)

机构地区：[1]济南市第二妇幼保健院药剂科,山东济南271100 [2]烟台市中医医院内科,山东烟台264013

出　　处：《中国现代医药杂志》2024年第10期13-18,共6页Modern Medicine Journal of China

摘　　要：目的探讨淫羊藿素对乳腺癌细胞上皮间质转化(EMT)的影响及可能的作用机制。方法采用不同浓度淫羊藿素干预MDA-MB-231细胞,采用划痕实验、Transwell实验、qRT-PCR检测法依次检测细胞侵袭能力、miR-200c表达水平及相关蛋白表达变化。结果MCF-7、MDA-MB-231、SK-BR-3细胞中miR-200c表达下降,其中以MDAMB-231细胞表达最低(P<0.05)。淫羊藿素可明显抑制MDA-MB-231细胞增殖,且随浓度增加对细胞抑制率明显增强。相较对照组、miR-200c NC组,miR-200c inhibitor组MDA-MB-231细胞迁移率升高,穿膜细胞数增加,β-catenin、Vimentin蛋白表达升高,miR-200c、E-cadherin蛋白表达降低(P<0.05);与对照组比较,淫羊藿素组细胞迁移率降低,穿膜细胞数减少,β-catenin、Vimentin蛋白表达降低,miR-200c、E-cadherin蛋白表达升高(P<0.05);与淫羊藿素组比较,淫羊藿素+miR-200c inhibitor组细胞迁移率升高,穿膜细胞数增加,β-catenin、Vimentin蛋白表达升高,miR-200c、E-cadherin蛋白表达降低(P<0.05)。结论淫羊藿素可阻断乳腺癌细胞的EMT过程,抑制肿瘤细胞的迁移、侵袭,其机制可能与上调miR-200c调控Wnt/β-catenin通路有关。Objective To investigate the effect of icariin on epithelial-mesenchymal transition(EMT)of breast cancer cells and its possible mechanism.Methods Different concentrations of icariin were used to treat MDAMB-231 cells.Scratch assay,Transwell assay,and qRT-PCR were used to sequentially detect cell invasion ability,miR-200c expression levels,and related protein expression changes.Results Compared with MCF-10A cells,miR-200c expression was significantly reduced in MCF-7,MDA-MB-231,and SK-BR-3 cells,with MDA-MB-231 cells showing the lowest expression(P<0.05).Icariin significantly inhibited the proliferation of MDA-MB-231 cells,and the cell inhibition rate increased significantly with increasing concentration.Compared with the control group and miR-200c NC group,the miR-200c inhibitor group and MDA-MB-231 cell healing rate increased,the number of transmembrane cells increased,the expression ofβ-catenin and Vimentin proteins increased,and the expression of miR-200c and E-cadherin proteins decreased(P<0.05).Compared with the control group,the icariin group showed a decrease in cell healing rate,a reduction in the number of transmembrane cells,a decrease in the expression ofβ-catenin and Vimentin proteins,and an increase in the expression of miR-200c and E-cadherin proteins(P<0.05).Compared with the icariin group,the icariin plus miR-200c inhibitor group showed an increase in cell healing rate,an increase in the number of transmembrane cells,an increase inβ-catenin and Vimentin protein expression,and a decrease in miR-200c and E-cadherin protein expression(P<0.05).Conclusion Icariin can block the EMT process of breast cancer cells,inhibit the migration and invasion of tumor cells.its mechanism may be related to the upregulation of miR-200c expression and the regulation of the Wnt/β-catenin signaling pathway.

关 键 词：乳腺癌 淫羊藿素 迁移 侵袭 上皮间质转化 MIR-200C 

分 类 号：R737.9[医药卫生—肿瘤]