Long non-coding RNA MALAT1 suppresses the proliferation and migration of endothelial progenitor cells in deep vein thrombosis by regulating the Wnt/β-catenin pathway.

Deep vein thrombosis (DVT) is one of the most common circulating vascular diseases with an incidence of ~0.1% worldwide. Although anticoagulant medication remains to be the main therapeutic approach for patients with DVT, existing thrombus and pulmonary embolisms still pose as a threat to patient life. Therefore, effective targeted therapies need to be developed and studies are required to improve understanding of this condition. Endothelial progenitor cells (EPCs) originate from the bone marrow, are located in the peripheral blood and are involved in thrombus resolution. Long non-coding RNAs (lncRNAs) are non-coding RNAs that are >200 nucleotides in length. LncRNAs are associated with the development of numerous vascular diseases. Among these lncRNAs, metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is downregulated in human atherosclerotic plaques. Furthermore, MALAT1 polymorphism resulted in vascular disease in Chinese populations. In the present study, the expression profile and potential functions of MALAT1 in DVT were investigated. The results revealed that MALAT1 was upregulated in DVT tissues. Furthermore, MALAT1 was able to regulate the biological behaviors of EPCs, including proliferation, migration, cell cycle arrest and apoptosis. In addition, the Wnt/β-catenin signaling pathway is a promising downstream target of MALAT1 in DVT. The changes in biological behaviors in EPCs caused by silenced MALAT1 were reversed by inhibition of the Wnt/β-catenin signaling pathway. In summary, the data indicated the roles of MALAT1 in the pathogenesis of DVT, and the MALAT1/Wnt/β-catenin axis could be a novel therapeutic target for the treatment of DVT.