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

Background: 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.

Methods: 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.

Results: 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.

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