tca cycle defects and cancer: when metabolism tunes redox state

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ID: 211549
2012
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Abstract
Inborn defects of the tricarboxylic acid (TCA) cycle enzymes have been known for more than twenty years. Until recently, only recessive mutations were described which, although resulted in severe multisystem syndromes, did not predispose to cancer onset. In the last ten years, a causal role in carcinogenesis has been documented for inherited and acquired alterations in three TCA cycle enzymes, succinate dehydrogenase (SDH), fumarate hydratase (FH), and isocitrate dehydrogenase (IDH), pointing towards metabolic alterations as the underlying hallmark of cancer. This paper summarizes the neoplastic alterations of the TCA cycle enzymes focusing on the generation of pseudohypoxic phenotype and the alteration of epigenetic homeostasis as the main tumor-promoting effects of the TCA cycle affecting defects. Moreover, we debate on the ability of these mutations to affect cellular redox state and to promote carcinogenesis by impacting on redox biology.
Reference Key
cardaci2012internationaltca Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Simone Cardaci;Maria Rosa Ciriolo
Journal Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
Year 2012
DOI
10.1155/2012/161837
URL
http://dx.doi.org/10.1155/2012/161837
Keywords
cytology

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