The signaling axis atypical protein kinase C λ/ι-Satb2 mediates leukemic transformation of B-cell progenitors View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

R. C. Nayak, S. Hegde, M. J. Althoff, A. M. Wellendorf, F. Mohmoud, J. Perentesis, M. Reina-Campos, D. Reynaud, Y. Zheng, M. T. Diaz-Meco, J. Moscat, J. A. Cancelas

ABSTRACT

Epigenetically regulated transcriptional plasticity has been proposed as a mechanism of differentiation arrest and resistance to therapy. BCR-ABL leukemias result from leukemic stem cell/progenitor transformation and represent an opportunity to identify epigenetic progress contributing to lineage leukemogenesis. Primary human and murine BCR-ABL+ leukemic progenitors have increased activation of Cdc42 and the downstream atypical protein kinase C (aPKC). While the isoform aPKCζ behaves as a leukemic suppressor, aPKCλ/ι is critically required for oncogenic progenitor proliferation, survival, and B-cell differentiation arrest, but not for normal B-cell lineage differentiation. In vitro and in vivo B-cell transformation by BCR-ABL requires the downregulation of key genes in the B-cell differentiation program through an aPKC λ/ι-Erk dependent Etv5/Satb2 chromatin repressive signaling complex. Genetic or pharmacological targeting of aPKC impairs human oncogenic addicted leukemias. Therefore, the aPKCλ/ι-SATB2 signaling cascade is required for leukemic BCR-ABL+ B-cell progenitor transformation and is amenable to non-tyrosine kinase inhibition. More... »

PAGES

46

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-018-07846-y

    DOI

    http://dx.doi.org/10.1038/s41467-018-07846-y

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1110955609

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30610188


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