MicroRNA-625-3p promotes the proliferation, migration and invasion of thyroid cancer cells by up-regulating astrocyte elevated gene 1

Abstract

BackgroundThyroid cancer is the most common malignancy in human endocrine system. This study aimed to investigate the effects of microRNA-625-3p (miR-625-3p) on thyroid cancer cell proliferation, migration, invasion and apoptosis, as well as underlying potential mechanism. MethodsThe relative expressions of miR-625-3p in tumor tissues and adjacent normal tissues of 20 patients with papillary thyroid cancer (PTC) were assessed using qRT-PCR. Cell transfection was used to up-regulate or down-regulate the expressions of miR-625-3p in thyroid cancer SW579 and TPC-1 cells. Effects of miR-625-3p overexpression or suppression on SW579 and TPC-1 cell viability, migration, invasion and apoptosis were detected respectively. The regulatory effect of miR-625-3p on astrocyte elevated gene 1 (AEG-1) expression was also analyzed. Then, the roles of AEG-1 in SW579 and TPC-1 cell proliferation, migration, invasion and apoptosis, as well as Wnt/β-catenin and c-Jun N-terminal kinase (JNK) pathways activation, were evaluated. ResultsmiR-625-3p had high expressions in tumor tissues, compared to adjacent normal tissues. Overexpression of miR-625-3p significantly promoted SW579 and TPC-1 cell proliferation, migration and invasion but had no influence on cell apoptosis. Knockdown of miR-625-3p had opposite effects, but induced cell apoptosis. AEG-1 was up-regulated by miR-625-3p overexpression and participated in the effects of miR-625-3p on SW-579 and TPC-1 cells. In addition, overexpression of AEG-1 induced the activation of Wnt/β-catenin and JNK pathways in SW579 and TPC-1 cells. ConclusionmiR-625-3p promoted proliferation, migration and invasion of thyroid cancer cells by enhancing the expression of AEG-1 and activating downstream Wnt/β-catenin and JNK pathways.