Antioxidant and oncogene rescue of metabolic defects caused by loss of matrix attachment

Zachary T. Schafer, Alexandra R. Grassian, Loling Song, Zhenyang Jiang, Zachary Gerhart-Hines, Hanna Y. Irie, Sizhen Gao, Pere Puigserver and Joan S. Brugge ()
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Zachary T. Schafer: Harvard Medical School, Boston, Massachusetts 02115, USA
Alexandra R. Grassian: Harvard Medical School, Boston, Massachusetts 02115, USA
Loling Song: Harvard Medical School, Boston, Massachusetts 02115, USA
Zhenyang Jiang: Harvard Medical School, Boston, Massachusetts 02115, USA
Zachary Gerhart-Hines: Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA
Hanna Y. Irie: Harvard Medical School, Boston, Massachusetts 02115, USA
Sizhen Gao: Harvard Medical School, Boston, Massachusetts 02115, USA
Pere Puigserver: Harvard Medical School, Boston, Massachusetts 02115, USA
Joan S. Brugge: Harvard Medical School, Boston, Massachusetts 02115, USA

Nature, 2009, vol. 461, issue 7260, 109-113

Abstract: Pro-cancer antioxidants There is laboratory evidence from in vitro and animal studies to suggest that antioxidants may suppress the development of cancer, though there is little conclusive evidence as to their effect in clinical conditions. Nevertheless it comes as something of a surprise to find that in certain conditions antioxidants can help promote cancer cell survival and proliferation. Normal epithelial cells die if they become detached from the structurally supportive extracellular matrix, but in breast cancer, cancer-causing genes such as ERBB2 can provide survival signals to detached tumorigenic cells. Schafer et al. show that cell detachment also causes metabolic defects that can be rescued both by ERBB2 and by antioxidants, which appear to act by boosting cellular energy levels via fatty acid oxidation. The findings point to novel mechanisms that could be exploited by cancer cells to enhance their survival in altered matrix environments.

Date: 2009
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DOI: 10.1038/nature08268

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