Regulation of Epidermal Growth Factor Receptor (EGFR) Expression by PML in Human Breast Cancer.
Abstract
Overexpression of epidermal growth factor receptor (EGFR), HER-2lneu, and myc oncogenes are some of the well described patterns of genetic changes that occur frequently in breast cancer. In addition, deletions of chromosomal loci that are thought to be associated with putative tumor suppressors and other genes, also contribute to more aggressive phenotype and metastasis of breast cancer. These genetic changes have important prognostic implication in the clinical outcome of breast cancer. Our laboratory is interested in exploring the role of PML, a novel tumor suppressor, on the regulation of EOFR expression in breast cancer. We show recently that PML suppresses the clonogenicity and tumorigenicity of cells derived from acute promyelocytic leukemia (APL). Furthermore, PML suppresses the transformation of REF and NIH3T3 cells by oncogenes. We also show that PML specifically represses the activity of EOFR gene promoter. These results suggest that PML is a tumor suppressor gene and that the chromosomal translocation in APL involving PML and retinoic acid receptor-a (RARa) disrupts the biological function of PML as a tumor suppressor. In the current study, we propose to investigate the interaction between PML and EOFR, and its consequence in the development of breast cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 15, 1995
- Accession Number
- ADA300274
Entities
People
- Khew-voon Chin
Organizations
- Robert Wood Johnson Medical School