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Transition state analogue of MTAP extends lifespan of APC^Min/+^ mice by Firestone, Ross S. (author);Feng, Mu (author);Basu, Indranil (author);Peregrina, Karina (author);Augenlicht, Leonard H. (author);Schramm, Vern L. (author) is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is Transition state analogue of MTAP extends lifespan of APC^Min/+^ mice about?

A mouse model of human Familial Adenomatous Polyposis responds favorably to pharmacological inhibition of 5′-methylthioadenosine phosphorylase (MTAP). Methylthio-DADMe-Immucillin-A (MTDIA) is an orally available, transition state analogue inhibitor of MTAP. 5′-Methylthioadenosine (MTA), the substrate for MTAP, is formed in polyamine synthesis and is recycled by MTAP to __S__-adenosyl-l-methionine (SAM) via salvage pathways. MTDIA treatment causes accumulation of MTA, which inhibits growth of human head and neck (FaDu) and lung (H359, A549) cancers in immunocompromised mouse models. We investigated the efficacy of oral MTDIA as an anti-cancer therapeutic for intestinal adenomas in immunocompetent APC^Min/+^ mice, a murine model of human Familial Adenomatous Polyposis. Tumors in APC^Min/+^ mice were decreased in size by MTDIA treatment, resulting in markedly improved anemia and doubling of mouse lifespan. Metabolomic analysis of treated mice showed no changes in polyamine, methionine, SAM or ATP levels when compared with control mice but indicated an increase in MTA, the MTAP substrate. Generation of an MTDIA-resistant cell line in culture showed a four-fold amplification of the meth

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It is typically read by researchers, students, and practitioners in Biochemistry, Genetics and Molecular Biology.

Author
Firestone, Ross S. (author);Feng, Mu (author);Basu, Indranil (author);Peregrina, Karina (author);Augenlicht, Leonard H. (author);Schramm, Vern L. (author)
Publisher
Springer Science and Business Media LLC
Published
2021
Language
EN
Field
Biochemistry, Genetics and Molecular Biology (Life Sciences)

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