Abstract
Accumulating evidence indicates that microRNAs function as oncogenes or tumor suppressor genes in human cancer. MiR-503 is deregulated in various human cancers and has been associated with hepatocellular carcinoma (HCC) progression. However, the underlying mechanisms of miR-503 involvement in the development and progression of HCC remains poorly understood. In the present study, we report that miR-503 suppresses cell metastasis in HCC through targeting the protein arginine methyl transferase 1 (PRMT1) mRNA. Notably, we identified that miR-503 was able to target 3′-untranslated region (3′-UTR) of PRMT1 mRNA by luciferase reporter gene assays. Then, we revealed that miR-503 was able to reduce the expression of PRMT1 at the levels of mRNA and protein using RT-PCR and Western blotting analysis. The expression levels of miR-503 were negatively related to those of PRMT1 mRNA in clinical HCC tissues. In terms of function, transwell and wound healing assays demonstrated that the miR-503 remarkably inhibited invasion and migration of HCC cells, which was reversed by overexpressed PRMT1. Furthermore, exogenous expression of miR-503 dramatically suppressed epithelial–mesenchymal transition (EMT) via PRMT1 in HCC cells. In conclusion, we denomstrated PRMT1 as a novel target gene of miR-503 and miR-503-mediated PRMT1 could also emerge as a potential important biomarker for HCC.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.