Format

Send to

Choose Destination
Drug Discov Today. 2017 May;22(5):796-804. doi: 10.1016/j.drudis.2016.12.003. Epub 2016 Dec 14.

Targeting amino acid metabolism for cancer therapy.

Author information

1
Department of Molecular Medicine, Cornell University, Ithaca, NY 14853, USA.
2
Department of Molecular Medicine, Cornell University, Ithaca, NY 14853, USA; Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY 14853, USA. Electronic address: rac1@cornell.edu.

Abstract

To support sustained biomass accumulation, tumor cells undergo metabolic reprogramming. Nutrient transporters and metabolic enzymes are regulated by the same oncogenic signals that drive cell-cycle progression. Some of the earliest cancer therapies used antimetabolites to disrupt tumor metabolism, and there is now renewed interest in developing drugs that target metabolic dependencies. Many cancers exhibit increased demand for specific amino acids, and become dependent on either an exogenous supply or upregulated de novo synthesis. Strategies to exploit such 'metabolic addictions' include depleting amino acids in blood serum, blocking uptake by transporters and inhibiting biosynthetic or catabolic enzymes. Recent findings highlight the importance of using appropriate model systems and identifying target patient groups as potential therapies advance into the clinic.

PMID:
27988359
PMCID:
PMC5429979
DOI:
10.1016/j.drudis.2016.12.003
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Elsevier Science Icon for PubMed Central
Loading ...
Support Center