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

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 were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effect...

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Veröffentlicht in:International journal of molecular medicine 2021-08, Vol.48 (2), p.1, Article 160
Hauptverfasser: Li, Ping, Li, Yuan, Chen, Lu, Ma, Xuexing, Yan, Xinxin, Yan, Meina, Qian, Buyun, Wang, Feng, Xu, Jingyi, Yin, Juan, Xu, Guidong, Sun, Kangyun
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container_title International journal of molecular medicine
container_volume 48
creator Li, Ping
Li, Yuan
Chen, Lu
Ma, Xuexing
Yan, Xinxin
Yan, Meina
Qian, Buyun
Wang, Feng
Xu, Jingyi
Yin, Juan
Xu, Guidong
Sun, Kangyun
description 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 were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effects of in CAD remain unknown. Therefore, the aim of the present study was to investigate the expression pattern and biological function of in CAD. First, 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 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 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 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 . Further experiments verified that regulated HUVEC proliferation and migration via . The results of the present study may enhance the current understanding of the role of lncRNA in CAD.
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In our previous study, the levels of lncRNA were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effects of in CAD remain unknown. Therefore, the aim of the present study was to investigate the expression pattern and biological function of in CAD. First, 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 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 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 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 . Further experiments verified that regulated HUVEC proliferation and migration via . 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In our previous study, the levels of lncRNA were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effects of in CAD remain unknown. Therefore, the aim of the present study was to investigate the expression pattern and biological function of in CAD. First, 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 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 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 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 . Further experiments verified that regulated HUVEC proliferation and migration via . 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In our previous study, the levels of lncRNA were upregulated in patients with CAD compared with those in control subjects. However, the role and underlying mechanism of the effects of in CAD remain unknown. Therefore, the aim of the present study was to investigate the expression pattern and biological function of in CAD. First, 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 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 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 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 . Further experiments verified that regulated HUVEC proliferation and migration via . The results of the present study may enhance the current understanding of the role of lncRNA in CAD.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>34212983</pmid><doi>10.3892/ijmm.2021.4993</doi><oa>free_for_read</oa></addata></record>
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source Spandidos Publications Journals; MEDLINE; Alma/SFX Local Collection; EZB Electronic Journals Library
subjects Adult
Aged
Aged, 80 and over
Analysis
Anticoagulants
Antisense RNA
Apoptosis
Atherosclerosis
Base Sequence
Biotechnology industry
Blood pressure
Cancer
Cardiovascular disease
Cell cycle
Cell Cycle - genetics
Cell Cycle Proteins - genetics
Cell Cycle Proteins - metabolism
Cell growth
Cell Movement - genetics
Cell Proliferation - genetics
Cells, Cultured
Coronary Artery Disease - genetics
Coronary Artery Disease - metabolism
Coronary Artery Disease - pathology
Coronary heart disease
Coronary vessels
Cyclin-dependent kinases
Development and progression
Disease prevention
Endothelium
Ethylenediaminetetraacetic acid
Female
Gene expression
Gene Expression Profiling - methods
Human Umbilical Vein Endothelial Cells - metabolism
Humans
Kinases
Male
Medical research
MicroRNA
MicroRNAs
MicroRNAs - genetics
Middle Aged
Plasma
RNA, Long Noncoding - genetics
RNA-Seq - methods
Scientific equipment and supplies industry
Sequence Homology, Nucleic Acid
title Long noncoding RNA uc003pxg.1 regulates endothelial cell proliferation and migration via miR‑25‑5p in coronary artery disease
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