Abstract
Metastasis is frequently observed in human follicular thyroid carcinoma. The present study investigated the peroxisome proliferator-activated receptor γ agonist, 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), and its effect on the migration of CGTH W-2 human thyroid carcinoma cells. 15d-PGJ2 decreased the survival rate of CGTH W-2 cells in a dose-dependent manner. The Transwell migration assay demonstrated that 15d-PGJ2 reduced the migration rate of CGTH W-2 cells by 35% following treatment with 30 µM 15d-PGJ2 compared with control cells. The cell adhesion assay indicated that, following 15d-PGJ2 treatment for 24 h, cell adhesion decreased by 26% compared with the control group. The expression levels of focal adhesion proteins, including integrin β1, phospho-focal adhesion kinase and p-paxillin, were downregulated following treatment with 15d-PGJ2. Immunostaining revealed that the puncta of vinculin were reduced and the actin stress fiber was disassembled following 15d-PGJ2 treatment. By contrast, p120-catenin (p120-ctn) and β-catenin levels staining accumulated in the region of the lamellipodium following 15d-PGJ2 treatment. Membrane fractionation revealed that p120-ctn and N-cadherin were decreased in the cell membrane, but increased in the cytoplasm of 15d-PGJ2-treated cells. Therefore, 15d-PGJ2 inhibited human thyroid carcinoma cell migration and this may be due to the impairment of focal adhesion complexes and the accumulation of p120-ctn in the cytoplasm in the region of the lamellipodium.