Upregulation of microRNA-206 induces apoptosis of vascular smooth muscle cells and decreases risk of atherosclerosis through modulating FOXP1

Forkhead box protein subfamily P (FOXP) 1 has an important role in the control of gene transcription and is also reported to function as a tumor suppressor. The aim of the present study was to explore the regulatory mechanisms of atherosclerosis by investigating the function of microRNA-206 (miR-206) and the regulatory association between miR-206 and its potential target gene, FOXP1, in vascular smooth muscle cells (VSMCs). Bioinformatics tools were utilized to identify FOXP1 as a target of miR-206. Luciferase reporter analysis was used to confirm this relationship and to identify the miR-206 binding site in the FOXP1 3'-untranslated region. It was demonstrated that the relative survival rate of VSMCs was suppressed by miR-206 compared with scramble controls. Furthermore, reduced expression of miR-206 in atherosclerosis tissue samples was observed, and the mRNA and protein expression levels of FOXP1 were upregulated in atherosclerosis tissue samples, both compared with the controls, indicating a negative correlation between miR-206 and FOXP1. Additionally, when treated with miR-206 mimics, the relative survival rate of VSMCs was notably reduced, which was rescued by overexpression of FOXP1. These findings increased the understanding of the regulatory role of miR-206 in atherosclerosis in VSMCs via targeting the FOXP1 gene; therefore, intervention with miR-206 as a therapeutic technique may be a strategy for atherosclerosis treatment in the future.