Protein arginine methyltransferase 1 promotes epithelial-mesenchymal transition via TGF-β1/Smad pathway in hepatic carcinoma cells.

Protein arginine methyltransferase 1 (PRMT1) is dysregulated in a number of human cancers. Herein, we report that PRMT1 expression is directly associated with epithelial-mesenchymal transition (EMT) in hepatic carcinoma cells. Firstly, we find that PRMT1 expression is higher in hepatic carcinoma tissues than that in normal liver tissues at both mRNA and protein levels, and higher expression of PRMT1 correlates with poor survival in liver tumors. The data in vitro reveals that PRMT1 knockdown inhibits the abilities of proliferation, migration and invasion, while PRMT1 overexpression promotes the above behaviors in hepatic carcinoma cells. Further studies indicate that PRMT1 knockdown remarkably decreases the expression of mesenchymal markers including Vimentin, Snail and N-cadherin, and upregulates expression of epithelial markers E-cadherin. Conversely, PRMT1 overexpression results in the opposite effects. Additionally, we identified that PRMT1 knockdown resulted in downregulation of TGF-β1, p-Smad2 and p-Smad3, while PRMT1 overexpression activated TGF-β1, p-Smad2 and p-Smad3. These findings suggest that PRMT1 promotes EMT in hepatic carcinoma cells probably via TGF-β1/Smad pathway, and might represent a novel anti-liver cancer strategy.