Identification of Surrogate Markers for Estrogen Receptor Action in Breast Cancer Cells

Abstract

Recent studies have described the identification of novel estrogen and antiestrogen inducible genes with interesting paradigms of regulation. However, due to the paucity of known estrogen receptor (ER) genomic targets, it is still not clear how estrogen displays mitogenic effects in the breast, and how these processes are dysregulated during the onset of hormone resistance. It is clear that the discovery of novel estrogen regulated genes will enable us to better define the key regulators of growth in ER-positive breast cancer cells. In the current study, differential display PCR was used to identify surrogate markers of estrogen and antiestrogen action in human breast cancer cells. A novel transcript was discovered that is upregulated by both the ER agonist l7beta-estradiol and the antagonist ICI l82,78O. The full length cDNA was cloned and identified as hMIP, the human homologue of the mitochondrial intermediate peptidase (hMIP), an enzyme important in cellular respiration. A second estrogen-responsive cDNA, encoding the control region of the mitochondrial genome, was also discovered. These studies highlight the role of ER pathways in mitochondrial function, and suggest that estrogen-stimulated mitogenesis in breast tissue may involve the enhancement of cellular processes of metabolism and energy generation.

Open PDF

Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2000
Accession Number
ADA388636

Entities

People

  • David Mcdonnell
  • Julianne Hall

Organizations

  • Duke University Hospital

Tags

DTIC Thesaurus Topics

  • Amino Acids
  • Biomedical And Dental Materials
  • Blood
  • Breast Cancer
  • Cell Line
  • Cells
  • Chemistry
  • Energy Production
  • Epithelial Cells
  • Gene Expression
  • Genetic Structures
  • Mrna
  • Neoplasms
  • Proteins
  • Ribonucleic Acids
  • Rodents
  • Tumor Cell Line

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Molecular Genetics