Tumor Specific Regulation of C-CAM Cell Adhesion Molecule in Prostate Cancer Carcinogenesis
Abstract
C-CAM is an epithelial cell adhesion molecule. We have shown that loss of C-CAM is an early event in prostate cancer development and re-introduction of C-CAM into prostate cancer cells could inhibit their tumorigenic potential. These results indicate that C-CAM is a tumor suppressor. The mechanism of C-CAM down-regulation in tumorigenesis is not clear. Our hypothesis is that transcriptional down-regulation instead of deletion of C-CAM gene is the major cause. We propose to identify mechanisms that regulate C-CAM gene expression in prostate carcinogenesis. We have identified that AP-2 is a transcriptional activator of C-CAM and thus is a potential regulator of C-CAM expression during tumorigenesis. In addition, we have developed a novel in vivo functional screening method to identify new transcription factors that regulate C-CAM gene expression during prostate carcinogenesis. Preliminary study has identified several candidate genes and we are in the process of confirming their effects on C-CAM expression. Our reviewer suggested that we pursue regulation of C-CAM gene expression by steroid hormones. We have incorporated androgen regulation in our study and have made significant progress in this effort. A manuscript is under submission. Results from this study will allow us to understand C-CAM gene regulation during tumorigenesis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2000
- Accession Number
- ADA390193
Entities
People
- Sue-hwa Lin
Organizations
- The University of Texas MD Anderson Cancer Center