| Literature DB >> 34799701 |
Mark R Sullivan1,2, Alicia M Darnell1,2, Montana F Reilly1, Tenzin Kunchok3, Lena Joesch-Cohen4, Daniel Rosenberg4, Ahmed Ali1,4, Matthew G Rees4, Jennifer A Roth4, Caroline A Lewis3, Matthew G Vander Heiden5,6,7,8.
Abstract
Folate metabolism can be an effective target for cancer treatment. However, standard cell culture conditions utilize folic acid, a non-physiological folate source for most tissues. We find that the enzyme that couples folate and methionine metabolic cycles, methionine synthase, is required for cancer cell proliferation and tumour growth when 5-methyl tetrahydrofolate (THF), the major folate found in circulation, is the extracellular folate source. In such physiological conditions, methionine synthase incorporates 5-methyl THF into the folate cycle to maintain intracellular levels of the folates needed for nucleotide production. 5-methyl THF can sustain intracellular folate metabolism in the absence of folic acid. Therefore, cells exposed to 5-methyl THF are more resistant to methotrexate, an antifolate drug that specifically blocks folic acid incorporation into the folate cycle. Together, these data argue that the environmental folate source has a profound effect on folate metabolism, determining how both folate cycle enzymes and antifolate drugs impact proliferation.Entities:
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Year: 2021 PMID: 34799701 PMCID: PMC8608285 DOI: 10.1038/s42255-021-00486-5
Source DB: PubMed Journal: Nat Metab ISSN: 2522-5812