Baicalin inhibits TGF-β1-induced epithelial-to-mesenchymal transition and suppresses pancreatic cancer cell migration and invasion

被引:0
|
作者
Zheng, Li [1 ]
Zhou, Zhongyong [1 ]
He, Zhikuan [1 ]
机构
[1] Henan Univ, Huaihe Hosp, Dept Gen Surg, 8 Baobei Rd, Kaifeng 475000, Henan, Peoples R China
关键词
Baicalin; pancreatic cancer; epithelial-to-mesenchymal transition (EMT); invasion; TGF-BETA; TUMOR PROGRESSION; GENE-EXPRESSION; E-CADHERIN; EMT; APOPTOSIS; TRANSDIFFERENTIATION; METASTASIS; CARCINOMA; PATHWAY;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The epithelial-mesenchymal transition (EMT) is an important cellular process during which epithelial polarized cells become motile mesenchymal-appeared cells, which, in turn, induces the metastasis of cancer. Baicalin is one of the main bioactive flavone glucuronides derived as a medical herb from the dried roots of Scutellaria baicalensis Georgi, and has been shown to possess anticancer activity. However, no detailed studies have so far been reported on its action on human pancreatic cancer. The aim of this study was to investigate the potential functions and molecular mechanisms of baicalin as an inhibitor of the transforming growth factor-beta 1 (TGF-beta 1)-induced EMT in human pancreatic cancer cells. In this study, we demonstrated that baicalin inhibited TGF-beta 1-induced EMT, as well as the expression of Snail and Slug in PANC-1 cells. Baicalin also inhibits cell migration and invasion during inhibition of TGF-beta 1-induced EMT. Moreover, baicalin inhibits phosphorylation of Smad2 and Smad3 during inhibition of TGF-beta 1-induced EMT. Taken together, our results showed that baicalin inhibited the TGF-beta 1-induced EMT and suppressed pancreatic cancer cell migration and invasion through inhibiting Smad signal pathway. Thus, baicaiinmay have potential as therapeutic or supplementary agents for the treatment of pancreatic
引用
收藏
页码:1054 / 1060
页数:7
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