Estrogen activates raf-1 kinase and induces expression of Egr-1 in MCF-7 breast cancer cells

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Updated: Jul 31, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

M A Pratt1, A Satkunaratnam, D M Novosad

  • 1Department of Pharmacology, University of Ottawa, Ontario, Canada.

Molecular and Cellular Biochemistry
|January 8, 1999
PubMed

Insights

Estrogen (E2) activates raf-1 kinase in estrogen receptor-positive breast cancer cells, leading to early growth response gene expression and influencing estrogen receptor signaling. This study reveals a key molecular pathway in breast cancer progression.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Estrogen receptor (ER) signaling is crucial in hormone-dependent breast cancers.
  • Raf-1 kinase is a key mediator in receptor tyrosine kinase and protein kinase C pathways.
  • The precise role of raf-1 kinase in estrogen-mediated breast cancer cell signaling requires further elucidation.

Purpose of the Study:

  • To investigate the activation of raf-1 kinase by estrogen (E2) in estrogen receptor-positive human breast cancer cells.
  • To examine the downstream effects of E2-induced raf-1 kinase activation on gene expression and ER signaling.

Main Methods:

  • MCF-7 cells were treated with estrogen (E2).
  • Raf-1 kinase autophosphorylation and electrophoretic mobility shift were analyzed.
  • Western blot analysis was used to detect raf-1 kinase activity.
  • Expression of early growth response gene-1 (Egr-1) mRNA and protein was quantified.
  • Transient transfection assays were performed to assess ER activation.

Main Results:

  • Estrogen (E2) treatment rapidly induced raf-1 kinase autophosphorylation and an electrophoretic mobility shift in MCF-7 cells.
  • E2 treatment led to increased expression of Egr-1 mRNA and protein, with kinetics similar to c-myc mRNA induction.
  • Activated raf-1 did not enhance ER transcriptional activity, but a dominant-negative raf-1 mutant inhibited E2-induced transcription.

Conclusions:

  • Estrogen (E2) activates raf-1 kinase in human breast cancer cells (MCF-7).
  • This activation is associated with the induction of early growth response genes like Egr-1.
  • Raf-1 kinase activity modulates estrogen receptor (ER) signaling, suggesting a role in breast cancer progression.

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