Fumarates and Cancer

Gwenny M Fuhler; Hester Eppinga; Maikel P Peppelenbosch

doi:10.1016/j.molmed.2016.12.001

Fumarates and Cancer

Trends Mol Med. 2017 Jan;23(1):3-5. doi: 10.1016/j.molmed.2016.12.001. Epub 2016 Dec 13.

Authors

Gwenny M Fuhler¹, Hester Eppinga², Maikel P Peppelenbosch²

Affiliations

¹ Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands. Electronic address: g.fuhler@erasmusmc.nl.
² Department of Gastroenterology and Hepatology, Erasmus MC University Medical Center, Rotterdam, The Netherlands.

PMID: 27986420
DOI: 10.1016/j.molmed.2016.12.001

Abstract

Accumulation of intermediate metabolites of the tricarboxylic acid (TCA) cycle in tumor cells can cause epithelial-to-mesenchymal transition (EMT), although the exact mechanisms remain elusive. Recent studies show that the oncometabolite fumarate, which accumulates in fumarate hydratase-deficient renal cancers, confers tumor aggressiveness by causing epigenetic changes in the antimetastatic miRNA cluster mir-200ba429. This may have important implications for the use of fumarates in the clinic.

Keywords: cancer; epithelial-to-mesenchymal transition; fumarate; metastasis.

MeSH terms

Animals
Citric Acid Cycle
Epigenesis, Genetic
Epithelial-Mesenchymal Transition
Fumarates / metabolism*
Humans
MicroRNAs / genetics
Neoplasm Metastasis / genetics
Neoplasm Metastasis / pathology
Neoplasms / genetics
Neoplasms / metabolism*
Neoplasms / pathology

Substances

Fumarates
MIRN200 microRNA, human
MicroRNAs