BTG2 Antiproliferative Gene and Prostate Cancer
Abstract
Expression of the protein product of the BTG2 tumor suppressor is lost during the transition of normal prostate epithelial cells into prostate cancer cells. Restoration of BTG2 expression in BTG2 null prostate cancer cells significantly reduces cell proliferation and tumorigenicity. Steady state levels of BTG2 protein are regulated post-translationally in p53 positive prostate cells. Our working hypothesis being tested as part of our proposed studies is that the tumor suppressive activity of BTG2 is lost as an early event in prostate carcinogenesis due to increased proteasomal degradation, leading to compromised cell cycle regulation, increased cell invasion and cancer progression. To date we have shown that BTG2 protein expression is lost as a very early event in prostate cancer and that prostate cancer tissue and cells degrade BTG2 at a greater rate than non-cancer tissue and cells. In the present reporting period we have shown that the subcellular localization and degradation kinetics of BTG2 are markedly regulated during the cell growth cycle. Specifically BTG2 is predominantly nuclear consistent with its antiproliferative function, but also BTG2 becomes concentrated in the nucleolus localization 4 hours following growth stimulation with EGF indicating that BTG2 might additionally influence some aspect of ribosome biosynthesis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Feb 01, 2006
- Accession Number
- ADA452471
Entities
People
- Paul D. Walden
Organizations
- Grossman School of Medicine