Han Jinming, Shen Xiaohan, Zhang Yong, Wang Suying, Zhou Leijie
Department of Spine Surgery, Ningbo No. 6 Hospital , Ningbo, Zhejiang, China.
Ningbo Diagnostic Pathology Center, Shanghai Cancer Center Ningbo Pathology Center, Ningbo Medical Center Lihuili Hospital , Ningbo, Zhejiang, China.
Biosci Biotechnol Biochem. 2020 Jul;84(7):1345-1352. doi: 10.1080/09168451.2020.1737502. Epub 2020 Mar 10.
Astragaloside IV (AS#IV) has previously demonstrated antitumoractivity. We investigated the effect and mechanisms of AS#IV in relation to epithelial-mesenchymal transition (EMT), viainterference with the Wnt/β-catenin signaling pathway in gliomaU251 cells. Induction of glioma U251 cells by transforming growthfactor (TGF)#β1 activated EMT, including switching E#cadherin toN-cadherin and altering the expression of Wnt/β-catenin signalingpathway components such as vimentin, β-catenin, and cyclin-D1.AS-IV inhibited the viability, invasion, and migration of TGF-β1-induced glioma U251 cells. AS-IV also interfered with the TGF#β1-induced Wnt/β-catenin signaling pathway in glioma U251 cells.These findings indicate that AS#IV prohibits TGF#β1-induced EMTby disrupting the Wnt/β-catenin pathway in glioma U251 cells. AS#IV may thus be a potential candidate agent for treating glioma andother central nervous system tumors.
黄芪甲苷IV（AS-IV）先前已显示出抗肿瘤活性。我们通过干扰胶质瘤U251细胞中的Wnt/β-连环蛋白信号通路，研究了AS-IV在上皮-间质转化（EMT）方面的作用及机制。转化生长因子（TGF）-β1诱导胶质瘤U251细胞发生EMT，包括E-钙黏蛋白向N-钙黏蛋白的转变以及波形蛋白、β-连环蛋白和细胞周期蛋白D1等Wnt/β-连环蛋白信号通路成分表达的改变。AS-IV抑制了TGF-β1诱导的胶质瘤U251细胞的活力、侵袭和迁移。AS-IV还干扰了胶质瘤U251细胞中TGF-β1诱导的Wnt/β-连环蛋白信号通路。这些发现表明，AS-IV通过破坏胶质瘤U251细胞中的Wnt/β-连环蛋白通路来抑制TGF-β1诱导的EMT。因此，AS-IV可能是治疗胶质瘤和其他中枢神经系统肿瘤的潜在候选药物。
