Loss of p300 accelerates MDS-associated leukemogenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-06

AUTHORS

G Cheng, F Liu, T Asai, F Lai, N Man, H Xu, S Chen, S Greenblatt, P-J Hamard, K Ando, X Chen, L Wang, C Martinez, M Tadi, L Wang, M Xu, F-C Yang, R Shiekhattar, S D Nimer

ABSTRACT

The role that changes in DNA methylation and histone modifications have in human malignancies is poorly understood. p300 and CREB-binding protein (CBP), two distinct but highly homologous lysine acetyltransferases, are mutated in several cancers, suggesting their role as tumor suppressors. In the current study, we found that deletion of p300, but not CBP, markedly accelerated the leukemogenesis ofNup98-HoxD13 (NHD13) transgenic mice, an animal model that phenotypically copies human myelodysplastic syndrome (MDS). p300 deletion restored the ability of NHD13 expressing hematopoietic stem and progenitor cells (HSPCs) to self-renew in vitro, and to expand in vivo, with an increase in stem cell symmetric self-renewal divisions and a decrease in apoptosis. Furthermore, loss of p300, but not CBP, promoted cytokine signaling, including enhanced activation of the MAPK and JAK/STAT pathways in the HSPC compartment. Altogether, our data indicate that p300 has a pivotal role in blocking the transformation of MDS to acute myeloid leukemia, a role distinct from that of CBP. More... »

PAGES

1382

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/leu.2016.347

DOI

http://dx.doi.org/10.1038/leu.2016.347

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1039700802

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27881875


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