Oncometabolites: Unconventional triggers of oncogenic signalling cascades.
Published version
Peer-reviewed
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Repository DOI
Type
Article
Change log
Authors
Sciacovelli, Marco
Frezza, Christian https://orcid.org/0000-0002-3293-7397
Abstract
Cancer is a complex and heterogeneous disease thought to be caused by multiple genetic lesions. The recent finding that enzymes of the tricarboxylic acid (TCA) cycle are mutated in cancer rekindled the hypothesis that altered metabolism might also have a role in cellular transformation. Attempts to link mitochondrial dysfunction to cancer uncovered the unexpected role of small molecule metabolites, now known as oncometabolites, in tumorigenesis. In this review, we describe how oncometabolites can contribute to tumorigenesis. We propose that lesions of oncogenes and tumour suppressors are only one of the possible routes to tumorigenesis, which include accumulation of oncometabolites triggered by environmental cues.
Description
Keywords
2-Hydroxyglutarate, Cancer, FH, Fumarate, IDH, Mitochondria, Oncometabolites, SDH, Succinate, Animals, Carcinogenesis, Citric Acid Cycle, Humans, Neoplasms, Signal Transduction
Journal Title
Free Radic Biol Med
Conference Name
Journal ISSN
0891-5849
1873-4596
1873-4596
Volume Title
100
Publisher
Elsevier BV
Publisher DOI
Sponsorship
MRC (unknown)
Medical Research Council (MC_UU_12022/6)
Medical Research Council (MC_UU_12022/6)
MS and CF are funded by an MRC Core Funding to the MRC Cancer Unit.