Nrdp1-Mediated ErbB3 Increase During Androgen Ablation and Its Contribution to Androgen-Independence
Abstract
In the past year, our laboratory has made significant strides towards the translation of observations made in the laboratory into clinical strategies that would help patients with prostate cancer. At the time of the last report, in a high profile article in Cancer Research, we had shown that ErbB3 is upregulated in prostate cancer cells undergoing androgen ablation, and this upregulation may be a major cause of the progression of prostate cancer to castration resistance. Now, using cell lines and animal models, we show that pharmaceutical inhibition of ErbB3 - achieved by dual inhibition of its binding partners EGFR and ErbB2, induce apoptosis and prevent survival to castration resistance. This paper has been very well received by the scientific community and has been featured at various websites. Another article - a review on ErbB3 in prostate cancer - has also been published. We are now preparing a fourth manuscript - one that describes Nrdp1 as a transcriptional target of AR, and shows that the AR binds to the proximal Nrdp1 promoter and promotes its transcription, only in castration sensitive, and not in castration resistant cells. This would complete four of the 5 tasks proposed in the grant.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2011
- Accession Number
- ADA552748
Entities
People
- Paramita M Ghosh
Organizations
- University of California