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Dai C. Metabolic stressors disrupt proteome homeostasis to suppress malignancy. Mol Cell Oncol. 2015;2(4)doi: 10.1080/23723556.2014.1002718.
Dai, C. (2015). Metabolic stressors disrupt proteome homeostasis to suppress malignancy. Molecular & cellular oncology, 2(4), . https://doi.org/10.1080/23723556.2014.1002718
Dai, Chengkai. "Metabolic stressors disrupt proteome homeostasis to suppress malignancy." Molecular & cellular oncology vol. 2,4 (2015). doi: https://doi.org/10.1080/23723556.2014.1002718
Dai C. Metabolic stressors disrupt proteome homeostasis to suppress malignancy. Mol Cell Oncol. 2015;2(4). doi: 10.1080/23723556.2014.1002718. Epub 2015 Jan 23. PMID: 26973866; PMCID: PMC4786015.
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Mol Cell Oncol. 2015;2(4). doi: 10.1080/23723556.2014.1002718. Epub 2015 Jan 23.

Metabolic stressors disrupt proteome homeostasis to suppress malignancy.

Molecular & cellular oncology

Chengkai Dai

Affiliations

  1. The Jackson Laboratory, Bar Harbor, ME 04609, USA.

PMID: 26973866 PMCID: PMC4786015 DOI: 10.1080/23723556.2014.1002718

Abstract

Within tumor cells the heat shock factor 1 (HSF1)-mediated stress response is constitutively mobilized to counter persistent proteotoxic stress, hence sustaining their fragile proteome homeostasis and supporting robust malignant phenotypes. Intriguingly, our new studies reveal that metabolic stressors, such as metformin, inactivate HSF1 and provoke proteomic chaos, thereby impeding tumorigenesis.

Keywords: AMPK; HSF1; glucose deprivation; metabolic stress; metformin; proteostasis; proteotoxic stress; tumor suppression; ubiquitination

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