Abstract
Abstract Background: Nucleotides 2-7 within mature miRNAs, short RNA molecule of between 19 and 22, create the ‘seed region’ that specifies the specific mRNA. To date, miRNAs have been linked to the etiology, progression and prognosis of cancer. The gain or loss of specific miRNAs can function as an oncogene or tumor suppressor. Design: By using recently developed miRNA 14K array (Agilent), we designed to compare miRNA expression between HRPCa cell line (PC3) and sensitive cell line (LNCaP). As validation for target mRNA following bioinformatics, candidates were applied on the neoadjuvant bicalutamide treated radical prostatectomized specimens using immunohistochemistry. Results: Amongst 57 upregulated miRNAs (ratio >2.0), oncomirs-miRNAs that are amplified or overexpressed in PC3, includes miR-31, -27a, -23a, -9, -100, -29a, -24, let 7i, -21, -221, 29b, -222, -181a. Probable candidates for target mRNAs to each oncomir are tumor suppressor gene family, including p27, PTEN, apoptosis related genes (DAXX, PDCD4, caspase recruitment domain 10/11), ECM adhesion genes (Integrin β4, ADAMTS 7/8), SOCS 6. In 23 downregulated miRNAs (ratio>2.0), tumor suppressor miRNAs that are downregualted or deleted from chromosomes acting as tumor suppressor genes, include miR-141, -200 a/b/c, -148a, -429, -34a, -195, -99a, -203, -125b-2. Possible candidates for target mRNAs are oncogeneic family are EMT-related genes including ZEB1, cell cycle related genes (Wee1, cyclin E1, CDK6), prostate specific proteins (STEAP1, prostein), RTK family (AXL, Rab-38, Rab-9A), transcriptional factor promotion (EIF2, SOX6), mitogen activator (MAP p38), secretory protein (SDF2). Among the top-listed candidates, STEAP1, prostein, ZEB1, and cyclin E1 were relatively overexpressed in the refractory PCa to compare with regressing cancer cells. Conclusion: Complicated networks of miRNA play substantial and crucial roles in the regulation of hormonal refractory prostate cancer, predominantly by virtue of STEAP1, prostein, ZEB1, cyclin E1 overexpression, and suppression of apoptosis-related genes. 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 5039. doi:1538-7445.AM2012-5039
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