Research Papers:
Baicalin inhibits the TGF-β1/p-Smad3 pathway to suppress epithelial-mesenchymal transition-induced metastasis in breast cancer
PDF | Full Text | How to cite
Metrics: PDF 1617 views | Full Text 2229 views | ?
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.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 27677