Modulation of Beta-catenin Activity With PKD1 Prostate Cancer
Abstract
During 2008-09 funding period we made considerable progress on our grant proposal and published one paper in Molecular Cancer Therapeutics. Our research findings were considered for highlight and appeared on cover page (cover illustration, MCT September 2008, volume 7). Along with publication three more papers were published from the lab. In next funding cycle we are expected to make progress on remaining specific aims and to have couple more publications. In brief, in 2008-09 funding period we have investigated the effect of bryostatin on PKD1 expression, beta-catenin transcription, cell proliferation, and cellular aggregation. In this study we examined the effect of Bryostatin 1 treatment on PKD1 activation, beta-catenin translocation and transcription activity and malignant phenotype of prostate cancer cells. Initial activation of PKD1 with Bryostatin 1 leads to colocalization of the cytoplasmic pool of beta-catenin with PKD1, trans-Golgi network markers and proteins involved in vesicular trafficking. Activation of PKD1 by Bryostatin 1 decreases nuclear beta-catenin expression and beta-catenin/TCF transcription activity. Activation of PKD1 alters cellular aggregation and proliferation in prostate cancer cells associated with subcellular redistribution of E-cadherin and beta-catenin. For the first time, we have identified Bryostatin 1 modulates beta-catenin signaling through PKD1, which identifies a novel mchansim to improve efficacy of Bryostatin 1 in clinical setting.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2009
- Accession Number
- ADA502884
Entities
People
- Meena Jaggi
- Subhash C. Chauhan