OBJECTIVE: The current study aimed to explore the roles of miR-31 and SOX11 in papillary thyroid carcinoma (PTC).
PATIENTS AND METHODS: Fifty-four paired human PTC specimens and matched normal thyroid tissues were obtained. Meanwhile, human thyroid epithelial cell Nthy-ori3-1 and PTC cells were cultured. The effects of miR-31 on PTC cell proliferation, invasion and migration were detected by cell proliferation assays and transwell assay, respectively. SOX11 expression in tissue samples was examined by immunohistochemical staining analyses (IHC). The correlation between SOX11 and miR-31 was clarified by Dual-Luciferase reporter assay. The relative mRNA and protein expression were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot. In addition, the xenograft model experiments were performed.
RESULTS: Declined miR-31 expressions were frequently identified in PTC, leading to poorer overall survival (OS) and worse clinicopathologic features of PTC patients. Moreover, functional assays indicated that miR-31 overexpression could notably repress PTC cell proliferation, invasion and migration abilities by regulating the extracellular regulated protein kinases (ERK) and protein kinase B (Akt) signaling pathways and epithelial-mesenchymal transition (EMT). In addition, the results of the Luciferase reporter assay demonstrated that SOX11 was a direct functional target of miR-31 in PTC cells. In vivo, miR-31 restoration significantly suppressed the tumor growth of xenograft PTC models.
CONCLUSIONS: Our findings indicated that miR-31 exerted anti-PTC functions via targeting SOX11 and modulating the ERK and Akt signaling pathways and EMT. MiR-31 may potentially serve as a novel biomarker in future therapeutics of PTC.Free PDF Download
To cite this article
Y. Wang, B.-G. Liu, C.-X. Zhou
MicroRNA-31 inhibits papillary thyroid carcinoma cell biological progression by directly targeting SOX11 and regulating epithelial-to-mesenchymal transition, ERK and Akt signaling pathways
Eur Rev Med Pharmacol Sci
Vol. 23 - N. 13