Antisense long non-coding RNA WEE2-AS1 regulates human vascular endothelial cell viability via cell cycle G(2)/M transition in arteriosclerosis obliterans

Long non-coding RNAs (lncRNAs) affect atherosclerosis by regulating the physiological and pathological processes of endothelial cells; however, the role of lncRNA WEE2 antisense RNA 1 (WEE2-AS1) in arteriosclerosis obliterans (ASO) is not completely understood. The present study aimed to explore the function of lncRNA WEE2-AS1 in human vascular endothelial cells. The results indicated that lncRNA WEE2-AS1 was significantly elevated in plasma and artery tissue samples of patients with ASO compared with healthy controls. The fluorescence in situ hybridization results suggested that lncRNA WEE2-AS1 was expressed in the cytoplasm and nuclei of primary human umbilical vein endothelial cells (HUVECs). The Cell Counting Kit-8 assay results suggested that lncRNA WEE2-AS1 knockdown significantly promoted HUVEC viability, whereas lncRNA WEE2-AS1 overexpression inhibited HUVEC viability compared with the negative control groups. Furthermore, analysis of the cell cycle by flow cytometry indicated that lncRNA WEE2-AS1 knockdown significantly decreased the proportion of cells in the G(0)/G(1) phase and significantly increased the proportion of cells in the G(2)/M phase compared with the negative control group. However, lncRNA WEE2-AS1 overexpression had no significant effect on cell cycle distribution compared with the negative control group. The western blotting results indicated that lncRNA WEE2-AS1 knockdown significantly reduced the expression levels of phosphorylated cyclin dependent kinase 1, WEE1 homolog 2 and myelin transcription factor 1, but increased the expression level of cell division cycle 25B compared with the negative control group. lncRNA WEE2-AS1 overexpression displayed the opposite effect on protein expression. Collectively, the present study suggested that lncRNA WEE2-AS1 was significantly upregulated in ASO and may serve a role in regulating human vascular endothelial cell viability. Further investigation into lncRNA WEE2-AS1 may broaden the current understanding of the molecular mechanism underlying ASO, and aid with the identification of specific probes and precise targeted drugs for the diagnosis and treatment of ASO.