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

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  • Zachary T. Schafer

    (Harvard Medical School, Boston, Massachusetts 02115, USA
    Present address: Department of Biological Sciences, University of Notre Dame, Notre Dame, Indiana 46556, 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
    Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, 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
    Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA)

  • Joan S. Brugge

    (Harvard Medical School, Boston, Massachusetts 02115, USA)

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.

Suggested Citation

  • Zachary T. Schafer & Alexandra R. Grassian & Loling Song & Zhenyang Jiang & Zachary Gerhart-Hines & Hanna Y. Irie & Sizhen Gao & Pere Puigserver & Joan S. Brugge, 2009. "Antioxidant and oncogene rescue of metabolic defects caused by loss of matrix attachment," Nature, Nature, vol. 461(7260), pages 109-113, September.
    • Handle: RePEc:nat:nature:v:461:y:2009:i:7260:d:10.1038_nature08268
    DOI: 10.1038/nature08268
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    Cited by:

    1. Jiaxin Liang & Deyang Yu & Chi Luo & Christopher Bennett & Mark Jedrychowski & Steve P. Gygi & Hans R. Widlund & Pere Puigserver, 2023. "Epigenetic suppression of PGC1α (PPARGC1A) causes collateral sensitivity to HMGCR-inhibitors within BRAF-treatment resistant melanomas," Nature Communications, Nature, vol. 14(1), pages 1-12, December.
    2. Rongli Sun & Meng Cao & Juan Zhang & Wenwen Yang & Haiyan Wei & Xing Meng & Lihong Yin & Yuepu Pu, 2016. "Benzene Exposure Alters Expression of Enzymes Involved in Fatty Acid β-Oxidation in Male C3H/He Mice," IJERPH, MDPI, vol. 13(11), pages 1-11, October.
    3. Karl K. Krull & Syed Azmal Ali & Jeroen Krijgsveld, 2024. "Enhanced feature matching in single-cell proteomics characterizes IFN-γ response and co-existence of cell states," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    4. Tal Levy & Kai Voeltzke & Laura Hruby & Khawla Alasad & Zuelal Bas & Marteinn Snaebjörnsson & Ran Marciano & Katerina Scharov & Mélanie Planque & Kim Vriens & Stefan Christen & Cornelius M. Funk & Chr, 2024. "mTORC1 regulates cell survival under glucose starvation through 4EBP1/2-mediated translational reprogramming of fatty acid metabolism," Nature Communications, Nature, vol. 15(1), pages 1-20, December.
    5. C. Megan Young & Laurent Beziaud & Pierre Dessen & Angela Madurga Alonso & Albert Santamaria-Martínez & Joerg Huelsken, 2023. "Metabolic dependencies of metastasis-initiating cells in female breast cancer," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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