Oncotarget

Research Papers:

Baicalin inhibits the TGF-β1/p-Smad3 pathway to suppress epithelial-mesenchymal transition-induced metastasis in breast cancer

Ding-Kuo Liu, Hui-Feng Dong, Rui-Fen Liu and Xi-Long Xiao _

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Oncotarget. 2020; 11:2863-2872. https://doi.org/10.18632/oncotarget.27677

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Abstract

Ding-Kuo Liu1, Hui-Feng Dong2, Rui-Fen Liu3,4 and Xi-Long Xiao1

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.


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