Abstract 5028: MicroRNA-212 targets multiple signaling pathways in prostate cancer

Abstract

Abstract Prostate cancer (PCa) is the most common type of cancer in men in the United States. While metastasis is the most common cause of death among PCa patients, no specific markers have been assigned to the severity of the disease. Identification of molecular factors could improve diagnosis and therapeutic intervention of PCa. MicroRNAs represent a promising new class of circulating biomarkers owing to their inherent stability and resilience. Studies in our lab have demonstrated that miR-212 is a differentially modulated circulatory microRNA in prostate cancer patients. Identification and validation of miRNA targets provides functional insights in mechanisms of prostate carcinogenesis and strategies for therapy. The present study was aimed to investigate and validate the targets for miR-212 to elucidate its role in prostate cancer and identify potential biomarkers and/or therapeutic targets for prostate cancer. Common mRNA targets of miR-212 were extracted from four web-based databases: TargetScan, miRanda, RNAhybrid, and PicTar. Some of the important common targets for miR-212 included DEDD, E2F5, GRM3, G2L1, SPRED1, SIRT1, SOS1, RASA1, PEA15, MYC, MAPK3, MAPK1 and HMGA2. Out of these SIRT1, SOS1, SPRED1, RASA1 were picked for further validation based on their documented role in carcinogenesis and tumor progression. Transfection studies with miR-212 mimics were performed in PC3 and LnCap prostate cancer cell lines. Western blotting was used to see the initial expression of various targets. 3′UTR-Luciferase reporter assay was performed for validating the target inhibition by miR-212. In addition, Cell proliferation assay and wound-healing assay were performed to evaluate the effects of miR-212 on PCa cell proliferation and migration. In summary the present study identifies and validates miR-212 targets and examines the functional significance of miR-212 in prostate cancer (PCa) cells lines. *Contributed equally. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 5028. doi:1538-7445.AM2012-5028