LINC01088 Targets miR-195-5p to Promote Proliferation and Migration and Reduce Apoptosis in the Inhibition of Carotid Artery Stenosis.

Abstract

Carotid artery stenosis (CAS) often goes undetected until it reaches an advanced stage, which can result in serious complications. The present study evaluated the potential of long noncoding RNA (lncRNA) LINC01088 as a biomarker for CAS. 92 CAS patients and 92 healthy controls (Control group) were included. RT-qPCR was performed to assess the relative levels of LINC01088 and miR-195-5p. Receiver operating characteristic (ROC) curve was used to evaluate the diagnostic potential of LINC01088. The relationship between LINC01088 and miR-195-5p was identified by luciferase reporter assay. Proliferation, migration, and apoptosis in human aortic endothelial cells (HAECs) were assessed using CCK8, transwell, and flow cytometry assay. DAVID was employed for Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses. CAS patients showed decreased LINC01088 expression and increased miR-195-5p expression compared to Control, with a negative correlation between their expression levels in CAS. LINC01088 demonstrated high sensitivity and specificity in distinguishing CAS patients from healthy individuals. LINC01088 directly targets miR-195-5p. Upregulation of LINC01088 reversed the effects of ox-LDL treatment, restoring proliferation and migration while reducing apoptosis in HAECs. However, miR-195-5p mimic reduced the protection of LINC01088 on HAECs proliferation, migration, and apoptosis. For miR-195-5p target genes, GO revealed protein metabolism pathways and KEGG highlighted the p53 and MAPK signaling pathways. The present study revealed the diagnosis value of LINC01088. LINC01088 reversed ox-LDL-induced proliferation, apoptosis, and migration by acting as sponges of miR-195-5p in HAECs. LINC01088 may serve as a protective biomarker in CAS progression.