Abstract
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. The present study aimed to investigate the regulatory effects and potential mechanisms of SNHG12 in human vascular smooth muscle cells (hVSMCs). Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) was employed to determine the expression of SNHG12, miR-766-5p and eukaryotic translation initiation factor 5A (EIF5A) 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-766-5p were predicted using starBase database and validated using luciferase reporter gene assays. Moreover, cell viability and migration were detected following EIF5A overexpression and SNHG12-knockdown. 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 EIF5A. EIF5A plasmids promoted the capacities of proliferation and migration in ox-LDL-induced hVSMCs. However, shRNA-SNHG12 counteracted the facilitation of EIF5A plasmids on hVSMCs biological behaviors. Taken together, these findings demonstrated that silencing of SNHG12 blocks the proliferation and migration of hVSMCs via targeting the miR-766-5p/EIF5A axis.
Highlights
Long non-coding RNAs have been reported to serve as potential biomarkers of atherosclerosis (AS), the role of long non-coding RNAs (lncRNAs) small nucleolar RNA host gene 12 (SNHG12) in AS still remains to be elucidated
ShRNA-SNHG12 counteracted the facilitation of eukaryotic translation initiation factor 5A (EIF5A) plasmids on human vascular smooth muscle cells (hVSMCs) biological behaviors
These findings demonstrated that silencing of SNHG12 blocks the proliferation and migration of hVSMCs via targeting the miR-766-5p/EIF5A axis
Summary
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. Small nucleolar RNA host gene 12 (SNHG12) is one of the classes of SNHGs.[7] Studies revealed that SNHG12 regulates cell proliferation, migration, invasion, and metastasis in several cancers,[8,9,10,11,12] indicating a potential target for cancer-directed interventions.[13] Except for its role in cancers, SNHG12 could ameliorate brain microvascular endothelial cell injury.[14] To date, a number of well-studied lncRNAs gave us important clues about their potential for AS treatment.[15] For instance, lincRNA-p21 is downregulated in atherosclerotic plaques of ApoE(−/−) mice, and it can suppress vascular smooth muscle cell (VSMC) proliferation and induce apoptosis.[16] HIF1α-AS1 regulates the proliferation and apoptosis of VSMCs.[17] The expression of H19 is higher in serum of AS patients,[18] serving as a potential biomarker for diagnosing AS. The status, biological function and regulatory mechanisms of SNHG12 in AS are still unknown
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