Role of PEPc, a Circular RNA Encoded Protein, in Castration-Resistant Prostate Cancer
Abstract
Prostate cancer contributes to the second most cancer related death for males in the United States. Almost all prostate cancer-related deaths can be attributed to failure of the cancer to respond to androgen ablation, or castration. A key molecule that drives this outcome in these patients is a well-known cancer gene: MYC. Unfortunately, patients affected by MYC-driven prostate cancers have fewer therapeutic options since MYC cannot be targeted with our current arsenal of drugs in prostate cancer patients. We have recently uncovered an important regulator of MYC, which is a long non-coding RNA named PVT1. We have shown that in cancer cells, if we switch off the activity of PVT1, it effectively eliminates MYC protein, which in turn renders cancer cells non-cancerous (Tseng et al. PVT1-dependence in cancer with MYC copy-number-increase. Nature, 2014, 512:82-86). The objective of this proposal is to investigate how exactly PVT1 enables MYC in prostate cancer patients. Our initial result points towards discovery of an interesting protein, PEPc, that we hypothesize to get coded only when the prostate cancer disease progresses. Here we propose to investigate this interesting finding and lay the grounds for developing molecules that can inhibit the ability of PEPc to stabilize MYC. This is likely to yield an innovative new therapy for treating castration-resistant prostate cancer patients. This study has very high likelihood in contributing to finding a cure for a significant proportion of these patients. While it may not directly end prostate cancer, it is very likely to contribute to developing effective therapies for patients and improving their chances for survival.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Aug 07, 2017
- Source ID
- W81XWH1710461
Entities
People
- Anindya Bagchi
Organizations
- Sanford Burnham Prebys Medical Discovery Institute
- United States Army