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Astragaloside IV (AS-IV) alleviates the malignant biological behavior of hepatocellular carcinoma via Wnt/β-catenin signaling pathway

机译:黄芪甲苷IV(AS-IV)通过Wnt /β-catenin信号通路减轻肝癌的恶性生物学行为

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Astragaloside IV (AS-IV) is an active substance isolated from Astragalus membranaceus (Fisch.) Bungede, which has been shown to have pharmacological effects in a variety of cancers. However, the effects of AS-IV in hepatocellular carcinoma (HCC) and its related mechanisms have been poorly understood. In this study, we explored the roles of AS-IV on HCC and the underlying signaling pathway. We reported that the appropriate concentrations of AS-IV (25, 50, 100 nmol l ~(?1) ) significantly suppressed the proliferation and cell cycle of HepG2 and Hep3B cell lines whilst promoting apoptosis. Besides, a trans-well and wound healing assay showed that AS-IV could markedly inhibit the migration and invasion of HepG2 and Hep3B cells, the expression of E-cadherin was up-regulation but the expression of N-cadherin and vimentin was down-regulation, and the protein levels of cleaved-caspase-3, 9 were increased markedly compared with the corresponding control. Furthermore, animal model treatment revealed that AS-IV could effectively reduce tumor formation. Moreover, AS-IV also significantly weakened the expression of Wnt, β-catenin and TCF-4 in vitro and in vivo . Taken together, these results suggested that AS-IV inhibited the biological processes of HCC via regulating of the Wnt/β-catenin pathway.
机译:黄芪甲苷IV(AS-IV)是一种从黄芪(Fisch。Bungede)分离的活性物质,已显示在多种癌症中具有药理作用。但是,人们对AS-IV在肝细胞癌(HCC)中的作用及其相关机制了解甚少。在这项研究中,我们探讨了AS-IV在肝癌中的作用和潜在的信号通路。我们报道了适当浓度的AS-IV(25、50、100nmol·(-1))可显着抑制HepG2和Hep3B细胞系的增殖和细胞周期,同时促进细胞凋亡。此外,通过穿刺孔和伤口愈合试验表明,AS-IV可以显着抑制HepG2和Hep3B细胞的迁移和侵袭,E-钙粘蛋白的表达上调,而N-钙粘蛋白和波形蛋白的表达下调。与相应的对照组相比,裂解的caspase-3、9的蛋白质水平显着增加。此外,动物模型治疗显示AS-IV可有效减少肿瘤形成。此外,在体外和体内,AS-IV还显着减弱了Wnt,β-catenin和TCF-4的表达。综上所述,这些结果表明,AS-IV通过调节Wnt /β-catenin途径抑制了HCC的生物学过程。

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