TAF1 plays a critical role in AML1-ETO driven leukemogenesis

Ye Xu, Na Man, Daniel Karl, Concepcion Martinez, Fan Liu, Jun Sun, Camilo Jose Martinez, Gloria Mas Martin, Felipe Beckedorff, Fan Lai, Jingyin Yue, Alejandro Roisman, Sarah Greenblatt, Stephanie Duffort, Lan Wang, Xiaojian Sun, Maria Figueroa, Ramin Shiekhattar and Stephen Nimer ()
Additional contact information
Ye Xu: University of Miami
Na Man: University of Miami
Daniel Karl: University of Miami
Concepcion Martinez: University of Miami
Fan Liu: University of Miami
Jun Sun: University of Miami
Camilo Jose Martinez: University of Miami
Gloria Mas Martin: University of Miami
Felipe Beckedorff: University of Miami
Fan Lai: University of Miami
Jingyin Yue: University of Miami
Alejandro Roisman: University of Miami
Sarah Greenblatt: University of Miami
Stephanie Duffort: University of Miami
Lan Wang: University of Miami
Xiaojian Sun: University of Miami
Maria Figueroa: University of Miami
Ramin Shiekhattar: University of Miami
Stephen Nimer: University of Miami

Nature Communications, 2019, vol. 10, issue 1, 1-15

Abstract: Abstract AML1-ETO (AE) is a fusion transcription factor, generated by the t(8;21) translocation, that functions as a leukemia promoting oncogene. Here, we demonstrate that TATA-Box Binding Protein Associated Factor 1 (TAF1) associates with K43 acetylated AE and this association plays a pivotal role in the proliferation of AE-expressing acute myeloid leukemia (AML) cells. ChIP-sequencing indicates significant overlap of the TAF1 and AE binding sites. Knockdown of TAF1 alters the association of AE with chromatin, affecting of the expression of genes that are activated or repressed by AE. Furthermore, TAF1 is required for leukemic cell self-renewal and its reduction promotes the differentiation and apoptosis of AE+ AML cells, thereby impairing AE driven leukemogenesis. Together, our findings reveal a role of TAF1 in leukemogenesis and identify TAF1 as a potential therapeutic target for AE-expressing leukemia.

Date: 2019
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-12735-z

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DOI: 10.1038/s41467-019-12735-z

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