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Updated: Sep 7, 2026

Mouse Mammary Epithelial Cells form Mammospheres During Lactogenic Differentiation
04:51

Mouse Mammary Epithelial Cells form Mammospheres During Lactogenic Differentiation

Published on: October 6, 2009

Epidermal growth factor receptor, platelet-derived growth factor receptor, and c-erbB-2 receptor activation all

D Taverna1, B Groner, N E Hynes

  • 1Friedrich Miescher Institute, Basel, Switzerland.

Cell Growth & Differentiation : the Molecular Biology Journal of the American Association for Cancer Research
|March 1, 1991
PubMed

Insights

Activation of epidermal growth factor (EGF) and c-erbB-2/neu receptors in HC11 cells promotes growth and prepares them for lactogenic hormone-induced differentiation. Platelet-derived growth factor (PDGF) receptor activation stimulates growth but not differentiation competence.

Area of Science:

  • Cell biology
  • Molecular endocrinology
  • Signal transduction

Background:

  • Mouse mammary epithelial cell line HC11 exhibits differentiation-specific functions.
  • Lactogenic hormones (glucocorticoids, prolactin) induce beta-casein expression, a marker of differentiation.
  • Receptor tyrosine kinases (RTKs) like EGF, c-erbB-2/neu, and PDGF are present in HC11 cells.

Purpose of the Study:

  • To investigate the effects of activating EGF, c-erbB-2/neu, and PDGF receptors on HC11 cell growth and differentiation.
  • To determine if RTK activation influences HC11 cell competence for lactogenic hormone response.

Main Methods:

  • Treatment of HC11 cells with epidermal growth factor (EGF), PDGF-BB, and lactogenic hormones.
  • Transfection of HC11 cells with an activated rat neuT receptor.
  • Analysis of beta-casein expression as a measure of differentiation.

Main Results:

  • EGF receptor activation enhanced cell growth and induced competence for lactogenic hormone response.
  • Activated neuT receptor (c-erbB-2/neu) conferred competence for lactogenic hormone response independently of EGF.
  • PDGF receptor activation stimulated cell growth but did not induce competence for lactogenic hormone response.
  • Optimal beta-casein synthesis required prior EGF exposure or neuT receptor activation.

Conclusions:

  • Activation of EGF and c-erbB-2/neu receptors, but not PDGF receptor, renders HC11 cells competent for optimal lactogenic hormone-induced differentiation.
  • Specific RTKs play distinct roles in regulating mammary epithelial cell growth and differentiation pathways.

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