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Interaction between fatty acid synthase- and ErbB-systems in ovarian cancer cells

Thomas W Grunt1, Renate Wagner, Michael Grusch

  • 1Signaling Networks Program, Department of Medicine I, Medical University Vienna, Vienna, Austria. thomas.grunt@meduniwien.ac.at

Biochemical and Biophysical Research Communications
|May 27, 2009
PubMed

Insights

Fatty acid synthase (FASN) and ErbB receptor inhibition synergize to treat ovarian cancer. Targeting both metabolic oncogenes and growth factor pathways offers a promising therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Fatty acid synthase (FASN) is a metabolic oncogene overexpressed in ovarian cancer.
  • FASN produces phospholipids, supporting membrane microdomains for receptor tyrosine kinases like EGFR and ErbB2.
  • Both FASN and ErbB receptors (EGFR, ErbB2) are frequently overexpressed in ovarian cancer.

Purpose of the Study:

  • To investigate the synergistic effects of inhibiting FASN and ErbB pathways in ovarian cancer cells.
  • To elucidate the molecular mechanisms underlying FASN and ErbB cooperation in ovarian cancer.

Main Methods:

  • Utilized ovarian cancer cell lines (A2780, SKOV3).
  • Performed growth assays to assess drug sensitivity.
  • Employed qRT-PCR and Western blotting to analyze gene and protein expression levels.

Main Results:

  • FASN inhibition (C75) sensitized ovarian cancer cells to multiple anti-ErbB drugs, indicating FASN/ErbB cooperation.
  • C75 treatment downregulated FASN, EGFR, ErbB2, and AKT expression.
  • AKT plays a crucial role in mediating the interaction between ErbB and FASN pathways.

Conclusions:

  • Combined inhibition of FASN and ErbB pathways abrogates their oncogenic functions in ovarian cancer.
  • Targeting FASN and ErbB receptors concurrently presents a viable therapeutic strategy for ovarian cancer treatment.

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