Histone deacetylase 1 plays a predominant pro-oncogenic role in Eμ-myc driven B cell lymphoma

The two histone deacetylases (Hdacs), Hdac1 and Hdac2, are erasers of acetylation marks on histone tails, and are important regulators of gene expression that were shown to play important roles in hematological malignancies. However, several recent studies reported opposing tumor-suppressive or tumo...

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Veröffentlicht in:Scientific reports Jg. 6; H. 1; S. 37772
Hauptverfasser: Pillonel, Vincent, Reichert, Nina, Cao, Chun, Heideman, Marinus R., Yamaguchi, Teppei, Matthias, Gabriele, Tzankov, Alexandar, Matthias, Patrick
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London Nature Publishing Group UK 25.11.2016
Nature Publishing Group
Schlagworte:
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13/2
13/31
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14/63
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45/29
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45/90
631/67/1990/291/1621/1915
631/80/458/1275
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Animals
Genes, myc
Histone Deacetylase 1 - metabolism
Histone Deacetylase 2 - metabolism
Humanities and Social Sciences
Humans
Lymphoma, B-Cell - genetics
Mice
multidisciplinary
Oncogenes
Science
ISSN:2045-2322, 2045-2322
Online-Zugang:Volltext
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Zusammenfassung:The two histone deacetylases (Hdacs), Hdac1 and Hdac2, are erasers of acetylation marks on histone tails, and are important regulators of gene expression that were shown to play important roles in hematological malignancies. However, several recent studies reported opposing tumor-suppressive or tumor-promoting roles for Hdac1 and Hdac2. Here, we investigated the functional role of Hdac1 and Hdac2 using the Eμ- myc mouse model of B cell lymphoma. We demonstrate that Hdac1 and Hdac2 have a pro-oncogenic role in both Eμ- myc tumorigenesis and tumor maintenance. Hdac1 and Hdac2 promote tumorigenesis in a gene dose-dependent manner, with a predominant function of Hdac1. Our data show that Hdac1 and Hdac2 impact on Eμ- myc B cell proliferation and apoptosis and suggest that a critical level of Hdac activity may be required for Eμ- myc tumorigenesis and proper B cell development. This provides the rationale for utilization of selective Hdac1 and Hdac2 inhibitors in the treatment of hematological malignancies.
Bibliographie:ObjectType-Article-1
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ObjectType-Feature-2
content type line 23
ISSN:2045-2322
2045-2322
DOI:10.1038/srep37772