Tumor Suppression and Sensitization to Taxol Induces Apoptosis of EIA in Breast Cancer Cells
Abstract
The purpose of this project is to study the molecular mechanisms underlying ElA's proapoptotic effect and anti-tumor activity and to dissect the functional domains of ElA that are critical for its antitumor activity. Because a phase I ElA gene therapy protocol for human breast and ovarian cancers was completed and a phase II clinical trial is undergoing, we also plan to develop an alternative ElA mutant construct to maximize ElA therapeutic effects while minimizing its potential side-effects for cancer gene therapy. In trying to understand the mechanism underlying ElA's antitumor activity, we have found that ElA downregulated VEGF expression both in vitro and in vivo, and mapped the domains required for this activity. We have also identified additional new target genes that were critically involved in El A-mediated chemosensitization and tumor suppression. In addition, I am planning to wire the panoramic signaling networks associated with ElA by systems biology approaches utilizing the genomic and proteomic technologies in an inducible ElA expression model system. These studies can provide useful information for us to better understand the molecular functions of ElA, and hopefully we can use this knowledge to better design a mutant ElA construct for cancer gene therapy in the future.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2005
- Accession Number
- ADA438490
Entities
People
- Yong Liao
Organizations
- The University of Texas MD Anderson Cancer Center