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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Epigenetic silencing of the myelopoiesis regulator microRNA-223 by the AML1/ETO oncoprotein.

Hematopoietic transcription factors are involved in chromosomal translocations, which generate fusion proteins contributing to leukemia pathogenesis. Analysis of patient's primary leukemia blasts revealed that those carrying the t(8;21) generating AML1/ETO, the most common acute myeloid leukemia-associated fusion protein, display low levels of a microRNA-223 (miR-223), a regulator of myelopoiesis. Here, we show that miR-223 is a direct transcriptional target of AML1/ETO. By recruiting chromatin remodeling enzymes at an AML1-binding site on the pre-miR-223 gene, AML1/ETO induces heterochromatic silencing of miR-223. Ectopic miR-223 expression, RNAi against AML1/ETO, or demethylating treatment enhances miR-223 levels and restores cell differentiation. Here, we identify an additional action for a leukemia fusion protein linking the epigenetic silencing of a microRNA locus to the differentiation block of leukemia.[1]

References

  1. Epigenetic silencing of the myelopoiesis regulator microRNA-223 by the AML1/ETO oncoprotein. Fazi, F., Racanicchi, S., Zardo, G., Starnes, L.M., Mancini, M., Travaglini, L., Diverio, D., Ammatuna, E., Cimino, G., Lo-Coco, F., Grignani, F., Nervi, C. Cancer. Cell (2007) [Pubmed]
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