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ERbB-2 expression is rate-limiting for epidermal growth factor-mediated stimulation of ovarian cancer cell

S S Hsieh1, C Malerczyk, A Aigner

  • 1Department of Pharmacology and Toxicology, Philipps-University Marburg, Germany.

International Journal of Cancer
|May 8, 2000
PubMed

Insights

Over-expression of ErbB-2 (ErbB-2 receptor tyrosine kinase) drives aggressive ovarian cancer by enhancing tumor cell proliferation. Targeting ErbB-2 may inhibit cancer growth, offering a potential therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Over-expression of the ErbB-2 proto-oncogene is linked to aggressive human adenocarcinomas.
  • ErbB-2 is a member of the ErbB family of growth factor receptors, forming preferential heterodimers within signaling networks.

Purpose of the Study:

  • To investigate if ErbB-2 is critical for epidermal growth factor (EGF)-mediated tumor cell proliferation.
  • To assess the role of EGFR-ErbB-2 heterodimers in ovarian cancer cell growth.

Main Methods:

  • Utilized SK-OV-3 ovarian cancer cells over-expressing EGF receptor (EGFR) and ErbB-2.
  • Reduced ErbB-2 expression using ribozyme transfection, creating cell lines with varying ErbB-2 levels.
  • Assessed anchorage-independent growth, EGF-induced proliferation, c-Fos mRNA expression, and spontaneous apoptosis.

Main Results:

  • ErbB-2 expression conferred a growth advantage and was rate-limiting for anchorage-independent growth.
  • EGF-induced colony formation was abrogated in ErbB-2-depleted cells, with unchanged EGFR levels and phosphorylation.
  • EGF-mediated c-Fos mRNA up-regulation duration decreased with ErbB-2 loss, and spontaneous apoptosis increased.

Conclusions:

  • The EGFR-ErbB-2 heterodimer, not the EGFR homodimer, is rate-limiting for EGF-mediated proliferation in ovarian cancer cells.
  • ErbB-2's oncogenic activity may stem from enhancing tumor cell response to EGF-like growth factors.
  • Targeting ErbB-2 could be a therapeutic strategy for ErbB-2-driven cancers.

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