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Protein Acetylation at the Interface of Genetics, Epigenetics and Environment in Cancer

1
Department of Pathology, Division of Pathological Neuroscience, Tokyo Women’s Medical University, Tokyo 162-8666, Japan
2
Ludwig Institute for Cancer Research, University of California San Diego, La Jolla, CA 92093, USA
3
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Amedeo Lonardo
Metabolites 2021, 11(4), 216; https://doi.org/10.3390/metabo11040216
Received: 3 March 2021 / Revised: 25 March 2021 / Accepted: 31 March 2021 / Published: 1 April 2021
Metabolic reprogramming is an emerging hallmark of cancer and is driven by abnormalities of oncogenes and tumor suppressors. Accelerated metabolism causes cancer cell aggression through the dysregulation of rate-limiting metabolic enzymes as well as by facilitating the production of intermediary metabolites. However, the mechanisms by which a shift in the metabolic landscape reshapes the intracellular signaling to promote the survival of cancer cells remain to be clarified. Recent high-resolution mass spectrometry-based proteomic analyses have spotlighted that, unexpectedly, lysine residues of numerous cytosolic as well as nuclear proteins are acetylated and that this modification modulates protein activity, sublocalization and stability, with profound impact on cellular function. More importantly, cancer cells exploit acetylation as a post-translational protein for microenvironmental adaptation, nominating it as a means for dynamic modulation of the phenotypes of cancer cells at the interface between genetics and environments. The objectives of this review were to describe the functional implications of protein lysine acetylation in cancer biology by examining recent evidence that implicates oncogenic signaling as a strong driver of protein acetylation, which might be exploitable for novel therapeutic strategies against cancer. View Full-Text
Keywords: metabolic reprogramming; microenvironment; protein acetylation; epigenetics; mechanistic target of rapamycin (mTOR) complexes metabolic reprogramming; microenvironment; protein acetylation; epigenetics; mechanistic target of rapamycin (mTOR) complexes
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MDPI and ACS Style

Harachi, M.; Masui, K.; Cavenee, W.K.; Mischel, P.S.; Shibata, N. Protein Acetylation at the Interface of Genetics, Epigenetics and Environment in Cancer. Metabolites 2021, 11, 216. https://doi.org/10.3390/metabo11040216

AMA Style

Harachi M, Masui K, Cavenee WK, Mischel PS, Shibata N. Protein Acetylation at the Interface of Genetics, Epigenetics and Environment in Cancer. Metabolites. 2021; 11(4):216. https://doi.org/10.3390/metabo11040216

Chicago/Turabian Style

Harachi, Mio, Kenta Masui, Webster K. Cavenee, Paul S. Mischel, and Noriyuki Shibata. 2021. "Protein Acetylation at the Interface of Genetics, Epigenetics and Environment in Cancer" Metabolites 11, no. 4: 216. https://doi.org/10.3390/metabo11040216

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