Baicalin inhibits the TGF-β1/p-Smad3 pathway to suppress epithelial-mesenchymal transition-induced metastasis in breast cancer
Ding-Kuo Liu, Hui-Feng Dong, Liu Rui-fen, Xilong Xiao
Abstract
// Ding-Kuo Liu 1 , Hui-Feng Dong 2 , Rui-Fen Liu 3 , 4 and Xi-Long Xiao 1 1 Department of Veterinary Medicine, China Agricultural University, Haidian District, Beijing, China 2 S&E Burgeoning Biotechnology (Tianjin) Co., Ltd, Wangwenzhuang Industrial Park, Xiqing District, Tianjin, China 3 Tianjin Key Laboratory of Microbial Preparation Enterprise for Feeding, Wangwenzhuang Industrial Park, Xiqing District, Tianjin, China 4 Tianjin Chinese Veterinary Medicine Technology Engineering Center, Huayuan Industrial Park, Tianjin, China Correspondence to: Xi-Long Xiao, email: [email protected] Keywords: baicalin; TGF-β1; p-Smad3; epithelial-mesenchymal transition; breast cancer Received: September 18, 2017     Accepted: February 26, 2018     Published: July 21, 2020 ABSTRACT TGF-β1 is an epithelial-mesenchymal transition (EMT)-inducing factor that is critical in tumor progression. However, whether the effect of TGF-β1 on breast cancer is through the EMT pathway remains to be determined, and drug development based on this mechanism needs to be improved. Results of this study showed that TGF-β1 dysregulation significantly correlated with the expression levels of EMT-associated markers and transcriptional factors. Exogenous expression of TGF-β1 promoted breast cancer cell metastasis and EMT progression. In addition, direct binding of baicalin to TGF-β1 caused its inactivation, which subsequently blocked signal transduction and inhibited breast cancer cell metastasis. In vivo experiment results further invalidated the inhibitory effect of baicalin on TGF-β1-induced tumor metastasis. These results suggest that baicalin, an active ingredient used in traditional Chinese medicine, exhibits a potential therapeutic effect on breast cancer metastasis by regulating TGF-β1-dependent EMT progression.