The methionine cycle and its cancer implications.
Autor: | Tassinari V; Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy., Jia W; Department of Pharmacology and Pharmacy, University of Hong Kong, Hong Kong, China., Chen WL; Cancer Institute, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200032, China., Candi E; Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy.; IDI-IRCCS, 00166, Rome, Italy., Melino G; Department of Experimental Medicine, TOR, University of Rome Tor Vergata, 00133, Rome, Italy. melino@uniroma2.it. |
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Jazyk: | angličtina |
Zdroj: | Oncogene [Oncogene] 2024 Nov; Vol. 43 (48), pp. 3483-3488. Date of Electronic Publication: 2024 Oct 11. |
DOI: | 10.1038/s41388-024-03122-0 |
Abstrakt: | The essential amino acid methionine is a crucial regulator of sulfur metabolism in a variety of interconnected biochemical pathways. The methionine cycle is intricately linked to the folate cycle, forming the one-carbon metabolism, a crucial regulator of S-adenosylmethionine, SAM. Recent work highlights methionine's critical role in tumor growth and progression, maintaining polyamine synthesis, and playing a crucial role in the regulation of SAM both in altered chromatin states, depending on p53 status, as well as facilitating m6A methylation of NR4A2 mRNA, hence regulating proliferation in esophageal carcinoma. Accordingly, Celecoxib, a specific NR4A2 inhibitor, is a potentially powerful inhibitor of tumor growth at least in this specific model. Additionally, formaldehyde, from endogenous or exogenous sources, can directly regulate both SAM steady-state-levels and the one-carbon metabolism, with relevant implication in cancer progression. These recent scientific advancements have provided a deeper understanding of the molecular mechanisms involved in cancer development, and its potential therapeutic regulation. Competing Interests: Ethics approval and consent to participate: Not applicable. Competing interests: GM is EBM in Oncogene. The authors declare no other conflict of interest. (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.) |
Databáze: | MEDLINE |
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