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Targeting fatty acid synthase: potential for therapeutic intervention in her-2/neu-overexpressing breast cancer

Javier A Menendez1, Ruth Lupu, Ramon Colomer

  • 1Department of Medicine, Evanston Northwestern Healthcare Research Institute, Evanston, Illinois 60201, USA. jmenendez@enh.org

Drug News & Perspectives
|October 26, 2005
PubMed

Insights

Fatty acid synthase (FAS) actively contributes to cancer by regulating the Her-2/neu oncogene. Inhibiting FAS impacts Her-2/neu activity, offering potential therapeutic strategies for breast cancer.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Fatty acid synthase (FAS)-catalyzed de novo fatty acid biosynthesis is an anabolic energy-storage pathway.
  • This pathway is increasingly recognized for its role in cancer development.
  • The Her-2/neu (erbB-2) oncogene is implicated in various cancers, particularly breast cancer.

Purpose of the Study:

  • To investigate the role of fatty acid synthase (FAS) in regulating the Her-2/neu oncogene in breast cancer.
  • To explore the correlation between FAS activity and Her-2/neu expression.
  • To determine the effects of modulating FAS activity on Her-2/neu oncoprotein.

Main Methods:

  • Analysis of human breast cancer cell lines for FAS expression and activity.
  • Assessment of Her-2/neu overexpression effects on FAS gene promoter activity.
  • Utilizing anti-Her-2/neu antibodies (trastuzumab) to inhibit FAS upregulation.
  • Employing pharmacological inhibitors to assess the impact on Her-2/neu activity.

Main Results:

  • A positive correlation was observed between high FAS levels and Her-2/neu amplification/overexpression in breast cancer cell lines.
  • Her-2/neu overexpression was found to stimulate FAS gene promoter activity, leading to increased fatty acid biosynthesis.
  • This Her-2/neu-induced FAS upregulation was successfully inhibited by trastuzumab.
  • Pharmacological inhibition of FAS activity resulted in negative regulation of Her-2/neu oncoprotein expression and tyrosine-kinase activity.

Conclusions:

  • Fatty acid synthase plays a significant role in the cancer phenotype by regulating the Her-2/neu oncogene.
  • The interaction between FAS and Her-2/neu is bidirectional, with Her-2/neu influencing FAS activity and vice versa.
  • Targeting FAS activity, potentially with agents like trastuzumab, presents a viable therapeutic strategy for Her-2/neu-driven cancers.

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