Galectin-3 Participation in the Epithelial-Mesenchymal Transition in Papillary Thyroid Carcinoma

Abstract

Background: Galectin-3 is the immunomarkers with strong specificity in the differential diagnosis of benign and malignant thyroid diseases. Galectin-3 could promote tumor progression through the Wnt pathway-mediated EMT. This study was aimed at investigating the effect of the interfering expression of the galectin-3 gene on the expression of transforming growth factor-β1 (TGF-β1)/Drosophila mothers against the decapentaplegic 3 (Smad3) and epithelial-mesenchymal transition (EMT)-related pro-teins in papillary thyroid carcinoma (PTC). Methods: Fifty cases of PTC andbenign thyroid tissues resected in our hospital were collected and the expressions of galectin-3, TGF-β1, and Smad3 proteins were detected via immunohistochemistry. The designed and synthesized small molecule interfering RNA (galectin-3-siRNA) was transfected in a TPC-1 cell line using the Lipofectamine2000 method, while the detection of the expressions of galectin-3, TGF-β1, Smad3, vimentin, and E-cadherin were achieved using the western blot method. Results: Compared with in the benign thyroid tissues, the galectin-3 and TGF-β1 were increased in the PTC tissues, while the Smad3 was reduced, with the difference statistically significant (p < 0.05). The galectin-3 was positively correlated with the TGF-β1 (r = 0.298, p = 0.036) and negatively correlated with the Smad3 in the PTC (r = –0.342, p = 0.015). Interference with the galectin-3 gene expression can down-regulate the expression of TGF-β1 and vimentin proteins and up-regulate the expression of Smad3 and E-cadherin proteins in TPC-1 cells (p < 0.05). Conclusions: Interfering with the galectin-3 gene expression can reduce the migration and invasion capacity of the TPC-1. Galectin-3 could promote the incidence of the EMT in PTC through the TGF-β1/Smad3 signaling pathway.