Silencing of lncRNA SNHG12 inhibits proliferation and migration of vascular smooth muscle cells via targeting miR-766-5p/EIF5A axis

Background. Although long non-coding RNAs (lncRNAs) have been reported to serve as potential biomarkers of atherosclerosis (AS), the role of lncRNA small nucleolar RNA host gene 12 (SNHG12) in AS still remains to be elucidated. Objectives. The present study aimed to investigate the regulatory effects and potential mechanisms of SNHG12 in human vascular smooth muscle cells (hVSMCs). Materials and methods. Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) was employed to determine the expression of SNHG12,miR-766-5p and eu karyotic translation initiation factor 5A (EIFSA) in oxidized low-density lipoprotein (ox-LDL)-induced hVSMCs. After transfection with short hairpin RNA (shRNA)-SNHG12, cell viability was estimated using the Cell Counting Kit-8 (CCK-8) assay. Wound healing and transwell assays were used for evaluating migratory capacities of hVSMCs. To further investigate the regulatory mechanisms, binding sites between SNHG12 and miR-766-5p, and EIF5A and miR-766-Sp were predicted using starBase data base a nd validated using luciferase reporter gene assays. Moreover, cell viability and migration were detected following EIF5A overexpression and SNHG12-knockdown. Results. SNHG12 was significantly upregulated in ox-LDL-induced hVSMCs. SNHG12 silencing inhibited ox-LDL-induced proliferation and migration of hVSMCs. Moreover, SNHG12 acted as a sponge of miR-766-5p, and miR-766-5p also interacted with EIFSA. EIFSA plasmids promoted the capacities of proliferation and migration in ox-LDL-induced hVSMCs. However, sh RNA-SNHG12 counteracted thefacilitation of EIF5A plasmids on hVSMCs biological behaviors. Conclusions. Taken together, these findings demonstrated that silencing of SNHG12 blocks the proliferation and migration of hVSMCs via targeting the miR-766-5p/EIF5A axis.