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Antisense long non-coding RNA WEE2-AS1 regulates human vascular endothelial cell viability via cell cycle G2/M transition in arteriosclerosis obliterans
- Source :
- Molecular Medicine Reports
- Publication Year :
- 2020
- Publisher :
- D.A. Spandidos, 2020.
-
Abstract
- 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 G0/G1 phase and significantly increased the proportion of cells in the G2/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.
- Subjects :
- Male
Cancer Research
Cell Survival
Cell
G2/M transition
Cell Cycle Proteins
WEE2 antisense RNA 1
Biochemistry
Flow cytometry
CDC2 Protein Kinase
Genetics
medicine
Human Umbilical Vein Endothelial Cells
Humans
RNA, Antisense
education
Molecular Biology
Aged
Cell Proliferation
Cyclin-dependent kinase 1
Gene knockdown
education.field_of_study
medicine.diagnostic_test
long non-coding RNA
Chemistry
viability
Cell Cycle
Endothelial Cells
Articles
Arteriosclerosis Obliterans
Cell cycle
Middle Aged
Protein-Tyrosine Kinases
Cell biology
Antisense RNA
Endothelial stem cell
G2 Phase Cell Cycle Checkpoints
MicroRNAs
medicine.anatomical_structure
Oncology
endothelial cell
Molecular Medicine
Female
RNA, Long Noncoding
atherosclerosis
Myelin transcription factor 1
Subjects
Details
- Language :
- English
- ISSN :
- 17913004 and 17912997
- Volume :
- 22
- Issue :
- 6
- Database :
- OpenAIRE
- Journal :
- Molecular Medicine Reports
- Accession number :
- edsair.doi.dedup.....125ec1f54d6ccae5b063d34d3752bf80