Estrogen and Myc negatively regulate expression of the EphA2 tyrosine kinase

J Cell Biochem. 2002;85(4):714-20. doi: 10.1002/jcb.10186.

Abstract

Estrogen receptor and c-Myc are frequently overexpressed during breast cancer progression but are downregulated in many aggressive forms of the disease. High levels of the EphA2 tyrosine kinase are consistently found in the most aggressive breast cancer cells, and EphA2 overexpression can increase metastatic potential. We demonstrate, herein, that estrogen and Myc negatively regulate EphA2 expression in mammary epithelial cells. These data reveal EphA2 as a downstream target of estrogen and Myc and suggest a mechanism by which estrogen and Myc may regulate breast cancer.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Breast / metabolism
  • Breast Neoplasms / genetics*
  • Breast Neoplasms / metabolism*
  • Cell Line
  • Epithelial Cells / metabolism
  • Estradiol / pharmacology
  • Estrogens / metabolism*
  • Female
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Neoplasms, Hormone-Dependent / genetics*
  • Neoplasms, Hormone-Dependent / metabolism*
  • Proto-Oncogene Proteins c-myc / metabolism*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / metabolism
  • Receptor Protein-Tyrosine Kinases / antagonists & inhibitors
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Receptor, EphA2
  • Receptors, Estrogen / metabolism
  • Tumor Cells, Cultured

Substances

  • Estrogens
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • RNA, Neoplasm
  • Receptors, Estrogen
  • Estradiol
  • Receptor Protein-Tyrosine Kinases
  • Receptor, EphA2