MiR-296-5p suppresses papillary thyroid carcinoma cell growth via targeting PLK1.

Our study aimed to explore the effects of miRNA-296-5p on the biological behaviors of papillary thyroid carcinoma (PTC) cells and its potential mechanism. Twenty-eight PTC tissues and the corresponding non-cancerous tissues were collected. Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) analysis was performed to detect the expression levels of miR-296-5p in PTC tissues and the adjacent non-cancerous tissues. Besides, the different endogenous expression levels of miR-296-5p in PTC cell line (K1) and normal thyroid gland cell line (Nthy-ori3-1) were also detected by RT-qPCR. Bioinformatics analysis, Western blot and Dual-Luciferase reporter gene assay were performed to demonstrate whether polo-like kinase 1 (PLK-1) was a downstream target of miR-296-5p. Subsequently, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay, flow cytometry analysis, colony formation assay and TUNEL assay were performed to estimate whether PLK1 down-regulation could attenuate the malignant behaviors of PTC cells in vitro. RT-qPCR results showed that the expression level of miR-296-5p was significantly down-regulated in PTC tissues and cells, indicating that miR-296-5p may participate in PTC development. We predicted target genes of miR-296-5p by bioinformatics and identified PLK1 as a target gene of miR-296-5p. By Western blot and Dual-Luciferase reporter gene assay, we confirmed that miR-296-5p was partially complement to PLKl mRNA 3'UTR sequence and inhibited PLK1 expression at the post-transcriptional level. In vitro experiments suggested that the transfection of miR-296-5p mimics into K1 cells suppressed cell proliferation, inhibited cell clone formation, arrest the cell cycle in G2/M phase and induced apoptosis. Importantly, PLK1 reversed the inhibitory effects of miR-296-5p on biological behaviors of PTC. MiR-296-5p influences the biological behaviors of PTC by regulating PLK1. These findings provide a new perspective for the molecular mechanism of PTC pathogenesis and also contribute to developing new targets and methods for PTC treatment.