miR-214 regulates papillary thyroid carcinoma cell proliferation and metastasis by targeting PSMD10

MicroRNAs (miRNAs) have important effects on cancer occurrence and development by adjusting gene expression. The aim of the present study was to examine the role of miR‑214 in papillary thyroid carcinoma cell proliferation and metastasis, and its molecular mechanisms. miR‑214 was demonstrated to be markedly downregulated in papillary thyroid carcinoma tissues and cells compared with normal, and this was significantly associated with lymph node metastasis, tumor size and TNM stage. Upregulation of miR‑214 significantly decreased cell proliferation, and promoted cell apoptosis and cell cycle arrest in papillary thyroid carcinoma cell lines in vitro. By contrast, downregulation of miR‑214 resulted in the opposite effects. In addition, miR‑214 mimics significantly decreased papillary thyroid carcinoma cell migration and invasion, which was correlated with decreased expression levels of matrix metallopeptidase (MMP)‑2 and MMP‑9. Restoration of miR‑214 expression in papillary thyroid carcinoma cells decreased the activities associated with epithelial‑mesenchymal transition (EMT). Furthermore, proteasome 26S subunit non‑ATPase 10 (PSMD10) was predicted to be a target of miR‑214. Experimental results demonstrated that miR‑214 negatively regulated PSMD10 expression by targeting its 3' untranslated region directly. Knockdown of PSMD10 reduced papillary thyroid carcinoma cell clone formation, migration and invasion, most likely by repressing glycogen synthase kinase (GSK)‑3β/β‑catenin and AKT signaling. Finally, a negative correlation was observed between the expression levels of miR‑214 and PSMD10 in papillary thyroid carcinoma tissues. Taken together, these data suggested that miR‑214 might be a candidate target for the treatment of papillary thyroid carcinoma.