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Ntziachristos, Panagiotis; Tsirigos, Aristotelis; Welstead, G Grant; Trimarchi, Thomas; Bakogianni, Sofia; Xu, Luyao; Loizou, Evangelia; Holmfeldt, Linda; Strikoudis, Alexandros; King, Bryan; Mullenders, Jasper; Becksfort, Jared; Nedjic, Jelena; Paietta, Elisabeth; Tallman, Martin S; Rowe, Jacob M; Tonon, Giovanni; Satoh, Takashi; Kruidenier, Laurens; Prinjha, Rab; Akira, Shizuo; Van Vlierberghe, Pieter; Ferrando, Adolfo A; Jaenisch, Rudolf; Mullighan, Charles G; Aifantis, Iannis
Nature (London), 10/2014, Letnik: 514, Številka: 7523Journal Article
T-cell acute lymphoblastic leukaemia (T-ALL) is a haematological malignancy with a dismal overall prognosis, including a relapse rate of up to 25%, mainly because of the lack of non-cytotoxic targeted therapy options. Drugs that target the function of key epigenetic factors have been approved in the context of haematopoietic disorders, and mutations that affect chromatin modulators in a variety of leukaemias have recently been identified; however, 'epigenetic' drugs are not currently used for T-ALL treatment. Recently, we described that the polycomb repressive complex 2 (PRC2) has a tumour-suppressor role in T-ALL. Here we delineated the role of the histone 3 lysine 27 (H3K27) demethylases JMJD3 and UTX in T-ALL. We show that JMJD3 is essential for the initiation and maintenance of T-ALL, as it controls important oncogenic gene targets by modulating H3K27 methylation. By contrast, we found that UTX functions as a tumour suppressor and is frequently genetically inactivated in T-ALL. Moreover, we demonstrated that the small molecule inhibitor GSKJ4 (ref. 5) affects T-ALL growth, by targeting JMJD3 activity. These findings show that two proteins with a similar enzymatic function can have opposing roles in the context of the same disease, paving the way for treating haematopoietic malignancies with a new category of epigenetic inhibitors.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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Vir: Osebne bibliografije
in: SICRIS
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