Abstract
ABSTRACT Transforming growth factor (TGF)-β1 plays a crucial role in the epithelial-to-mesenchymal transition (EMT) in many cancer types and in thyroid cancers. Epigallocatechin-3-gallate (EGCG), the most important ingredient in the green tea, has been reported to possess antioxidant and anticancer activities. However, the cellular and molecular mechanisms explaining its action have not been completely understood. In this study, we found that EGCG significantly suppresses EMT, invasion and migration in anaplastic thyroid carcinoma (ATC) 8505C cells in vitro by regulating the TGF-β/Smad signaling pathways. EGCG significantly inhibited TGF-β1-induced expression of EMT markers (E-cadherin reduction and vimentin induction) in 8505C cells in vitro. Treatment with EGCG completely blocked the phosphorylation of Smad2/3, translocation of Smad4. Taken together, these results suggest that EGCG suppresses EMT and invasion and migration by blocking TGFβ/Smad signaling pathways.
Highlights
Transforming growth factor β (TGF-β), a ubiquitously expressed cytokine, may act as both a tumor suppressor and a potent stimulator of tumor progression, local invasion, and metastasis [1]
This study is the first to demonstrate that EGCG inhibits TGF-β1-induced epithelial to mesenchymal transition (EMT) in 8505C cells
We found that the inhibitory effects of EGCG on TGF-β1-induced epithelial to mesenchyme transition (EMT) may be related to inhibition of the TGF-β1-mediated signaling pathways Smad2/3/4
Summary
Transforming growth factor β (TGF-β), a ubiquitously expressed cytokine, may act as both a tumor suppressor and a potent stimulator of tumor progression, local invasion, and metastasis [1]. Loss of E-cadherin expression is a hallmark of Clinically evident indicated that 50% of ATC patients have had distant metastases at the time of clinical diagnosis, as to the ATC patients who have not had distant metastases They will be classified as stage IV by the American Joint Committee on Cancer. In papillary thyroid carcinoma and ATC cells, EMT was induced by TGF-β1 and increased tumor invasiveness in PTCs [14,15]. These data indicated that targeting TGF-β1 expression could reversed EMT and inhibited ATC cells invasion
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