MicroRNA-26a suppresses the malignant biological behaviors of papillary thyroid carcinoma by targeting ROCK1 and regulating PI3K/AKT signaling pathway

摘要

OBJECTIVE: Papillary thyroid carcinoma (PTC) is an endocrine malignancy, the morbidity of which has kept rising in recent years. MicroRNA (miRNA/miR) is emerging as a key regulator in carcinogenesis, including PTC. The current study concentrates on the biological roles and mechanisms of miR-26a in the PTC progression. PATIENTS AND METHODS: 51 pairs of PTC tissue samples and matched adjacent thyroid tissues were collected from PTC patients who received surgical excisions at The People’s Hospital of Linqing between July 2015 and June 2018 with informed consent. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect expressions of miR-26a and rho-associated coiled-coil–containing protein kinase 1 (ROCK1) mRNA in PTC tissues and cells. Functional assays, including (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) MTT assays and transwell assays were performed to determine the roles of miR-26a in the PTC progression. Western blot was used to detect expression levels of the related proteins. RESULTS: Findings demonstrated prominently down-regulated miR-26a in PTC tissues and cells. Down-regulated miR-26a indicated malignant clinicopathologic characteristics and shorter overall survival rate of PTC patients. MTT assay and transwell assay indicated that miR-26a up-regulation significantly repressed PTC cell viability, invasion, and metastasis. Western blot analysis revealed that miR-26a exerted its anti-PTC effects via phosphatidylinositol 3-kinase/protein kinase B pathway (PI3K/AKT) and epithelial-to-mesenchymal transition (EMT). ROCK1 was a target of miR-26a in PTC cells and ROCK1 was mediated by miR-26a, as a regulatory mechanism in PTC. CONCLUSIONS: Taken together, these findings demonstrated the anti-tumor functions of miR-26a in PTC, providing novel strategies for PTC diagnosis and therapy.