Long noncoding RNA uc003pxg.1 regulates endothelial cell proliferation and migration via miR‑25‑5p in coronary artery disease

Ping Li; Yuan Li; Lu Chen; Xuexing Ma; Xinxin Yan; Meina Yan; Buyun Qian; Feng Wang; Jingyi Xu; Juan Yin; Guidong Xu; Kangyun Sun

doi:10.3892/ijmm.2021.4993

Long noncoding RNA uc003pxg.1 regulates endothelial cell proliferation and migration via miR‑25‑5p in coronary artery disease

Int J Mol Med. 2021 Aug;48(2):160. doi: 10.3892/ijmm.2021.4993. Epub 2021 Jul 2.

Authors

Ping Li¹, Yuan Li², Lu Chen², Xuexing Ma², Xinxin Yan¹, Meina Yan¹, Buyun Qian², Feng Wang¹, Jingyi Xu¹, Juan Yin¹, Guidong Xu², Kangyun Sun²

Affiliations

¹ Department of Central Laboratory, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu 215008, P.R. China.
² Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu 215008, P.R. China.

Abstract

Long noncoding RNAs (lncRNAs) have been reported to be associated with the progression of coronary artery disease (CAD). In our previous study, the levels of lncRNA uc003pxg.1 were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effects of uc003pxg.1 in CAD remain unknown. Therefore, the aim of the present study was to investigate the expression pattern and biological function of uc003pxg.1 in CAD. First, uc003pxg.1 expression levels were assessed in peripheral blood mononuclear cells isolated from patients with CAD by reverse transcription‑quantitative (RT‑q)PCR. The results demonstrated that the levels of uc003pxg.1 were significantly upregulated (~4.6‑fold) in samples from 80 patients with CAD compared with those in 80 healthy subjects. Subsequently, the present study demonstrated that small interfering RNA‑mediated uc003pxg.1 knockdown inhibited human umbilical vein endothelial cell (HUVEC) proliferation and migration, which was analyzed using the Cell Counting Kit‑8, cell cycle, EdU and Transwell assays. Additionally, the results of RT‑qPCR and western blot analyses revealed that uc003pxg.1 regulated the mRNA and protein levels of cyclin D1 and cyclin‑dependent kinase. Through high‑throughput sequencing and dual‑luciferase reporter assays, the present study demonstrated that microRNA (miR)‑25‑5p was a downstream target of uc003pxg.1. Further experiments verified that uc003pxg.1 regulated HUVEC proliferation and migration via miR‑25‑5p. The results of the present study may enhance the current understanding of the role of lncRNA uc003pxg.1 in CAD.

Keywords: cell proliferation and migration; coronary artery disease; long noncoding RNA; peripheral blood mononuclear cells.

MeSH terms

Adult
Aged
Aged, 80 and over
Base Sequence
Cell Cycle / genetics
Cell Cycle Proteins / genetics
Cell Cycle Proteins / metabolism
Cell Movement / genetics*
Cell Proliferation / genetics*
Cells, Cultured
Coronary Artery Disease / genetics*
Coronary Artery Disease / metabolism
Coronary Artery Disease / pathology
Female
Gene Expression Profiling / methods
Human Umbilical Vein Endothelial Cells / metabolism*
Humans
Male
MicroRNAs / genetics*
Middle Aged
RNA, Long Noncoding / genetics*
RNA-Seq / methods
Sequence Homology, Nucleic Acid

Substances

Cell Cycle Proteins
MIRN25 microRNA, human
MicroRNAs
RNA, Long Noncoding

Grants and funding

This work was supported by the Special Diagnosis Techniques for Clinical Key Diseases of Suzhou Municipal Health and Family Planning Commission (grant no. LCZX201910), the Science and Technology Development Fund of Nanjing Medical University (grant no. NMUB2018219), The Natural Science Foundation of Jiangsu Province for Youth (grant no. BK20190189) and the Youth Program of National Natural Science Foundation of China (grant no. 82000379).