Abstract
Abstract Introduction and Objective: The Wnt/beta-catenin (CTNNB1) and Ras-Raf-MEK-ERK signaling pathway play an important role in bladder cancer progression. Tumor suppressive miRNAs targeting these cancer pathways may provide a new therapeutic approach for bladder cancer. Methods: We initially identified miRNA-1826 potentially targeting CTNNB1, VEGFC, MEK1 using several target scan algorithms. The expression of miR-1826 was confirmed in bladder cancer tissues and bladder cancer cell lines. Then we performed several functional analyses of miR-1826. Finally 3′UTR luciferase assay and Western blot were performed to look at relationship between miR-1826 and target genes. Results: MiR-1826 expression was significantly lower in bladder cancer tissues and bladder cancer cell lines (J82, T24, TCC-SUP) compared to normal bladder tissues and normal bladder cell lines (SV-HUC-1). The expression of miR-1826 was lower in bladder cancer tissues and inverse correlation of miR-1826 with several clinical parameters (pT, grade) was observed. The functional analyses showed that miR-1826 inhibited bladder cancer cell viability, invasion and migration. Also we also found increased apoptosis and G1 cell cycle arrest in miR-1826 transfected bladder cancer cells. 3′UTR luciferase activity and protein expression of these target genes (CTNNB1, MEK1, VEGFC) were significantly down-regulated in miR-1826 transfected bladder cancer cells (J82, T24). To examine whether the effect of miR-1826 was through CTNNB1 (beta-catenin) or MEK1 knock down, we knocked down CTNNB1/MEK1 mRNA using a si-RNA technique. We observed that CTNNB1 or MEK1 siRNA knockdown resulted in effects similar to those with miR-1826 in bladder cancer cells. Conclusions: Our data suggests that the miR-1826 plays an important role as tumor suppressor via CTNNB1/MEK1/VEGFC down-regulation in bladder cancer. 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 2293. doi:1538-7445.AM2012-2293
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: 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.
