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Updated: May 17, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
[EGCG regulates TGF-β1-induced epithelial mesenchymal transition in squamous cell carcinoma of head and neck]
Lei-ming Pi1, Yong Liu, Chang-yun Yu
1Department of Otorhinolaryngology, Central South University, Changsha, China.
Objective:
To study the effect and molecular mechanism of epigallocatechin-3-gallate (EGCG) on epithelial-mesenchymal transition (EMT) in vitro induced by human recombinant TGF-β1 protein in squamous cell carcinoma of the head and neck.
Methods:
EMT morphological changes of Tu686 cells were observed after sequential treatment of 5 ng/ml TGF-β1 and 20 µmol/L EGCG. Tu686 cells were collected after the treatment of 5 ng/ml TGF-β1 for 24 h and EGCG with different concentrations (0, 10, 20, 30 µmol/L) for another 24 h or 20 µmol/L EGCG treatment for different time phase (6, 12, 24 h). Then RT-PCR and Western-blot were applied to detect mRNA and protein expression level of epithelial cell marker E-cadherin, mesenchymal cell marker Vimentin and Smad7, an inhibit molecule of TGF-β1 mediated pathway in Tu686 cells.
Results:
TGF-β1 successfully induced characterized EMT morphological and molecular changes in Tu686 cells, in which expression of E-cadherin decreased, Vimentin increased and Smad7 declined. However, EGCG could reverse the TGF-β1 mediated process of EMT by downregulating the expression of Vimentin and upregulating the expression of E-cadherin and Smad7.
Conclusion:
EGCG significantly inhibits TGF-β1-mediated EMT inTu686 cell lines of SCCHN, which maybe associated with the upregulated-expression of Smad7, an inhibitor in TGF-β1 signaling pathway.
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