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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Vydáno v:Scientific reports Ročník 6; číslo 1; s. 37772
Hlavní autoři: Pillonel, Vincent, Reichert, Nina, Cao, Chun, Heideman, Marinus R., Yamaguchi, Teppei, Matthias, Gabriele, Tzankov, Alexandar, Matthias, Patrick
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 25.11.2016
Nature Publishing Group
Témata:
13
13/1
13/2
13/31
13/51
14/63
38/77
45/29
45/41
45/90
631/67/1990/291/1621/1915
631/80/458/1275
64/60
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
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Shrnutí: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.
Bibliografie:ObjectType-Article-1
SourceType-Scholarly Journals-1
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content type line 23
ISSN:2045-2322
2045-2322
DOI:10.1038/srep37772