Cells demand methionine not only for protein synthesis but still for nucleotide synthesis, methylation, and reductive absorption, and indeed, these pathways support the extreme proliferative rate of cancer cells. Although various drugs (for example, methotrexate) that upset the methionine cycle have long been secondhand for cancer situation, they showed solid side effects. Therefore, developing a more recent generation of drugs accompanying minimal side effects should to treat cancer. Methionine is an essential amino acid treated through the methionine and folate cycle, and these pathways also produce two essential cellular antioxidants: hydrogen sulfide (H2S) and glutathione (GSH). Due to the extreme proliferative rate, cancer containers depend on these pathways for methylation and the production of H2S and GSH to claim cellular equilibrium. On the other hand, due to the overuse of methionine, tumor cells still generate oxidative stress via the overdone production of homocysteine (Hcy). However, malignancy cells handle this oxidative stress by way of the overproduction of H2S and GSH. This article widely discussed the methionine adding in cancer cells and in what way or manner we can exploit this dependency on methionine to create a newer generation of drugs accompanying minimal reactions.
Author(s) Details:
Avisek Majumder,
Department of Medicine, University of California, San Francisco, CA 94143, USA.
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