15-Deoxy-Δ-prostaglandin J inhibits migration of human thyroid carcinoma cells by disrupting focal adhesion complex and adherens junction.

Metastasis is frequently observed in human follicular thyroid carcinoma. The present study investigated the peroxisome proliferator-activated receptor γ agonist, 15-deoxy-Δ-prostaglandin J (15d-PGJ), and its effect on the migration of CGTH W-2 human thyroid carcinoma cells. 15d-PGJ decreased the survival rate of CGTH W-2 cells in a dose-dependent manner. The Transwell migration assay demonstrated that 15d-PGJ reduced the migration rate of CGTH W-2 cells by 35% following treatment with 30 µM 15d-PGJ compared with control cells. The cell adhesion assay indicated that, following 15d-PGJ 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-PGJ. Immunostaining revealed that the puncta of vinculin were reduced and the actin stress fiber was disassembled following 15d-PGJ treatment. By contrast, p120-catenin (p120-ctn) and β-catenin levels staining accumulated in the region of the lamellipodium following 15d-PGJ treatment. Membrane fractionation revealed that p120-ctn and N-cadherin were decreased in the cell membrane, but increased in the cytoplasm of 15d-PGJ-treated cells. Therefore, 15d-PGJ 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.