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Green, Alexa S.; Chapuis, Nicolas; Trovati Maciel, Thiago; Willems, Lise; Lambert, Mireille; Arnoult, Christophe; Boyer, Olivier; Bardet, Valerie; Park, Sophie; Foretz, Marc; Viollet, Benoit; Ifrah, Norbert; Dreyfus, François; Hermine, Olivier; Cruz Moura, Ivan; Lacombe, Catherine; Mayeux, Patrick; Bouscary, Didier; Tamburini, Jerome
Blood, 11/2010, Letnik: 116, Številka: 20Journal Article
Finding an effective treatment for acute myeloid leukemia (AML) remains a challenge, and all cellular processes that are deregulated in AML cells should be considered in the design of targeted therapies. We show in our current study that the LKB1/AMPK/TSC tumor suppressor axis is functional in AML and can be activated by the biguanide molecule metformin, resulting in a specific inhibition of mammalian target of rapamycin (mTOR) catalytic activity. This induces a multisite dephosphorylation of the key translation regulator, 4E-BP1, which markedly inhibits the initiation step of mRNA translation. Consequently, metformin reduces the recruitment of mRNA molecules encoding oncogenic proteins to the polysomes, resulting in a strong antileukemic activity against primary AML cells while sparing normal hematopoiesis ex vivo and significantly reducing the growth of AML cells in nude mice. The induction of the LKB1/AMPK tumor-suppressor pathway thus represents a promising new strategy for AML therapy.
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in: SICRIS
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