miR-125-5p inhibits thyroid cancer growth and metastasis by suppressing the ERK/PI3K/AKT signal pathway

Background Thyroid cancer is one of the most common endocrine malignant tumors. The study has found that microRNA-125-5p (miR-125-5p) is regarded as a key regulator of gene expression and involved in cancer cell growth by affecting the miRNA-mediated signal pathway. It is crucial to understand the potential mechanism of miR-125-5p in regulating thyroid tumor cell proliferation and metastasis. Objective To investigate biological functions of miR-125-5p in thyroid cancer growth and metastasis and explored potential mechanism mediated by miR-125-5p in thyroid cancer cells. Methods Western blot, gene transfection, flow cytometry, immunohistochemistry were used to analyze the regulatory effects of miR-125-5p in thyroid cancer cells. Result Results observed that miR-125-5p expression was down-regulated in thyroid cancer tissue compared to adjacent normal tissue. miR-125-5p overexpression inhibited thyroid cancer cell growth, migration and invasion. miR-125-5p overexpression arrested thyroid cancer cell cycle at S phase, and significantly induced apoptosis of thyroid cancer cells. miR-125-5p overexpression increased the protein levels of extracellular regulated protein kinase (ERK), phosphatidylinositol 3 kinase (PI3K) and phosphoinositide dependent kinase (AKT) while it decreased protein expression of phosphorylated ERK, PI3K and AKT in thyroid cancer cells. In vivo assay demonstrated that miR-125-5p transfection inhibited tumor growth and ERK, PI3K and AKT protein expression in tumor tissues. Conclusion In summary, these results indicate that miR-125-5p can inhibit thyroid cancer cell growth, migration and invasion through the ERK/PI3K/AKT signaling pathway.