PTEN inhibits epithelial mesenchymal transition of thyroid cancer cells by regulating the Wnt/β-Catenin signaling pathway

ObjectiveThe global incidence of thyroid cancer (THCA) has significantly risen in recent years. This study aims to investigate the role and mechanisms of PTEN in epithelial mesenchymal transition (EMT), invasion and migration of THCA cells.MethodsPTEN expression in THCA was analyzed through bioinformatics databases. RT-qPCR and Western blot analyses were performed to quantify PTEN levels in the Nthy-ori 3-1 cell line and three THCA cell types (TPC-1, B-CPAP, FTC-133). TPC-1 cells were transfected with a PTEN overexpression plasmid and treated with the Wnt activator. Cell viability and apoptosis were assessed via CCK-8 and flow cytometry, respectively. The expression levels of E-Cadherin, N-Cadherin, and Vimentin in TPC-1 cells were evaluated using Western blot. The invasive, migratory, and wound-healing abilities of the cells were examined using Transwell and scratch assays. Activation of the Wnt/beta-catenin pathway was assessed through Western blot.ResultsPTEN expression was significantly lower in THCA cells, particularly in TPC-1 cells compared to other cell lines. PTEN overexpression led to decreased viability in TPC-1 cells, increased apoptosis, and a rise in E-Cadherin levels while reducing N-Cadherin and Vimentin levels, thereby inhibiting EMT. Furthermore, PTEN overexpression diminished the invasive, migratory and wound-healing capabilities of TPC-1 cells and suppressed activation of the Wnt/beta-catenin pathway. Treatment with the Wnt activator partially counteracted the effects of PTEN overexpression on TPC-1 cells.ConclusionPTEN functions to inhibit EMT and the invasive and migratory characteristics of THCA cells by blocking the activation of the Wnt/beta-catenin pathway.