Apoptosis-Dependent and Apoptosis-Independent Functions of Bim in Prostate Cancer Cells
Abstract
Attenuated apoptotic response and extended cell survival have been implicated in prostate cancer (PCa) development and progression. We recently found that Bim, a BH3-only pro-apoptotic protein, is upregulated in PCa cells in vitro and in vivo. The main objective of this postdoctoral fellowship is to elucidate why PCa cells upregulate Bim and what is the role of the upregulated Bim proteins in modulating PCa cell behavior (death, survival, proliferation/division, etc.). Our hypothesis is that, under normal, unstimulated conditions, with its apoptotic function blocked, the upregulated Bim in PCa cells plays an apoptosis-independent function(s). Under apoptosis-stimulated conditions, however, Bim can still participate in triggering a robust apoptotic response, thus guaranteeing that weaker or more susceptible PCa cells be eliminated from the population. Two Specific Aims were proposed to determine: 1) apoptosis-independent functions of the upregulated Bim in PCa cells under unstimulated conditions, and 2) apoptosis-dependent functions of the upregulated Bim in PCa cells under stimulated conditions. The PI of the grant, Dr. Junwei Liu, had to leave the lab Oct. of 2004. Before he left, he had completed all experiments in Specific Aim 2 with one manuscript published (Append. I). After he left, with the small amounts of funds left over from the Fellowship, we have just accomplished all of the experiments proposed in Specific Aim 1 and are in the process of preparing a manuscript, which will be supplied to DOD when it is ready.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2005
- Accession Number
- ADA467615
Entities
People
- Dean Tang
- Junwei Liu
Organizations
- The University of Texas MD Anderson Cancer Center