Homozygous MTAP deletion in primary human glioblastoma is not associated with elevation of methylthioadenosine

Homozygous MTAP deletion in primary human glioblastoma is not associated with elevation of methylthioadenosine

The metabolite methylthioadenosine (MTA) inhibits PRMT5. Therefore, MTA accumulation due to MTA phosphorylase (MTAP) deletion has been proposed as a vulnerability for PRMT5-targeted therapy in cancer. Here, the authors show that MTA does not accumulate in MTAP-deficient cancer cells but is secreted...

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Autores principales: Yasaman Barekatain, Jeffrey J. Ackroyd, Victoria C. Yan, Sunada Khadka, Lin Wang, Ko-Chien Chen, Anton H. Poral, Theresa Tran, Dimitra K. Georgiou, Kenisha Arthur, Yu-Hsi Lin, Nikunj Satani, Elliot S. Ballato, Eliot I. Behr, Ana C. deCarvalho, Roel G. W. Verhaak, John de Groot, Jason T. Huse, John M. Asara, Raghu Kalluri, Florian L. Muller
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Science
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Acceso en línea:https://doaj.org/article/52cd1479712f4a068ae698d7e4c9858e
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Sumario:The metabolite methylthioadenosine (MTA) inhibits PRMT5. Therefore, MTA accumulation due to MTA phosphorylase (MTAP) deletion has been proposed as a vulnerability for PRMT5-targeted therapy in cancer. Here, the authors show that MTA does not accumulate in MTAP-deficient cancer cells but is secreted and metabolized by MTAP-intact cells in the tumour microenvironment.

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