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.