EGCG regulates TGF-β1-induced epithelial mesenchymal transition in squamous cell carcinoma of head and neck.
- Author:
Lei-ming PI
1
;
Yong LIU
;
Chang-yun YU
;
Geng-ming CAI
;
Dong-hai HUNAG
;
Yuan-zheng QIU
;
Yong-quan TIAN
;
Xin ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Cadherins; metabolism; Carcinoma, Squamous Cell; metabolism; Catechin; analogs & derivatives; pharmacology; Cell Line, Tumor; Epithelial-Mesenchymal Transition; drug effects; Head and Neck Neoplasms; metabolism; Humans; Signal Transduction; drug effects; Smad7 Protein; metabolism; Transforming Growth Factor beta1; metabolism; Vimentin; metabolism
- From: Chinese Journal of Otorhinolaryngology Head and Neck Surgery 2012;47(9):749-752
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODSEMT 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.
RESULTSTGF-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.
CONCLUSIONEGCG 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.