LncRNA CASC2 mediates the lower extremity deep vein thrombosis via sponging miR-152-3p

Lower extremity deep vein thrombosis (DVT) is a prevalent form of peripheral vascular disease, notable for its high incidence rate. We investigated the potential mechanisms through which the long non-coding RNA (lncRNA) CASC2/miR-152-3p axis regulates the DVT.

150 patients diagnosed with DVT and 150 controls were included. CASC2 and miR-152-3p levels were quantified using RT-qPCR. HUVECs viability was assessed via the CCK-8 assay, while cell migration was evaluated using Transwell chamber assays. Flow cytometry was employed to determine cell apoptosis. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), ICAM, and VCAM concentrations were measured through ELISA. The interaction between lncRNA CASC2 and miR-152-3p was validated using a dual-luciferase reporter assay. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were conducted for function and pathway enrichment.

LncRNA CASC2 was significantly downregulated in DVT patients. LncRNA CASC2 was independently associated with the occurrence of DVT and demonstrated a relatively high diagnostic value. Overexpression of lncRNA CASC2 significantly enhanced HUVEC's proliferation and migration, while reducing apoptosis and the concentrations of TNF-α, IL-1β, IL-6, ICAM-1, and VCAM-1. Conversely, the knockdown of lncRNA CASC2 resulted in opposite effects. LncRNA CASC2 directly targeted and negatively regulated miR-152-3p. Additionally, miR-152-3p counteracted the effects of lncRNA CASC2 on cell function. GO and KEGG analyses revealed that the target genes of miR-152-3p were mainly involved in the TGF-β and PI3K-Akt signaling pathways.

The lncRNA CASC2/miR-152-3p axis played a critical role in mediating the formation of DVT.