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The putative tumor suppressor gene EphA7 is a novel BMI-1 target

Prost, Gaëlle LU ; Braun, Sebastian LU ; Hertwig, Falk LU ; Winkler, Marcus LU ; Jagemann, Lucas LU ; Nolbrant, Sara LU ; Leefa, Isabelle V. LU ; Offen, Nils LU ; Miharada, Kenichi LU and Lang, Stefan LU orcid , et al. (2016) In Oncotarget 7(36). p.58203-58217
Abstract

Bmi1 was originally identified as a gene that contributes to the development of mouse lymphoma by inhibiting MYC-induced apoptosis through repression of Ink4a and Arf. It codes for the Polycomb group protein BMI-1 and acts primarily as a transcriptional repressor via chromatin modifications. Although it binds to a large number of genomic regions, the direct BMI-1 target genes described so far do not explain the full spectrum of BMI-1-mediated effects. Here we identify the putative tumor suppressor gene EphA7 as a novel direct BMI-1 target in neural cells and lymphocytes. EphA7 silencing has been reported in several different human tumor types including lymphomas, and our data suggest BMI1 overexpression as a novel mechanism leading to... (More)

Bmi1 was originally identified as a gene that contributes to the development of mouse lymphoma by inhibiting MYC-induced apoptosis through repression of Ink4a and Arf. It codes for the Polycomb group protein BMI-1 and acts primarily as a transcriptional repressor via chromatin modifications. Although it binds to a large number of genomic regions, the direct BMI-1 target genes described so far do not explain the full spectrum of BMI-1-mediated effects. Here we identify the putative tumor suppressor gene EphA7 as a novel direct BMI-1 target in neural cells and lymphocytes. EphA7 silencing has been reported in several different human tumor types including lymphomas, and our data suggest BMI1 overexpression as a novel mechanism leading to EphA7 inactivation via H3K27 trimethylation and DNA methylation.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Bmi1, EphA7, neural stem cells, DNA methylation
in
Oncotarget
volume
7
issue
36
pages
15 pages
publisher
Impact Journals
external identifiers
  • scopus:84988416847
  • wos:000387153200061
  • pmid:27533460
ISSN
1949-2553
DOI
10.18632/oncotarget.11279
language
English
LU publication?
yes
id
4fb50f28-60c8-40ad-9dae-c23d774cbb27
date added to LUP
2017-06-13 12:48:04
date last changed
2024-01-13 22:47:19
@article{4fb50f28-60c8-40ad-9dae-c23d774cbb27,
  abstract     = {{<p>Bmi1 was originally identified as a gene that contributes to the development of mouse lymphoma by inhibiting MYC-induced apoptosis through repression of Ink4a and Arf. It codes for the Polycomb group protein BMI-1 and acts primarily as a transcriptional repressor via chromatin modifications. Although it binds to a large number of genomic regions, the direct BMI-1 target genes described so far do not explain the full spectrum of BMI-1-mediated effects. Here we identify the putative tumor suppressor gene EphA7 as a novel direct BMI-1 target in neural cells and lymphocytes. EphA7 silencing has been reported in several different human tumor types including lymphomas, and our data suggest BMI1 overexpression as a novel mechanism leading to EphA7 inactivation via H3K27 trimethylation and DNA methylation.</p>}},
  author       = {{Prost, Gaëlle and Braun, Sebastian and Hertwig, Falk and Winkler, Marcus and Jagemann, Lucas and Nolbrant, Sara and Leefa, Isabelle V. and Offen, Nils and Miharada, Kenichi and Lang, Stefan and Artner, Isabella and Nuber, Ulrike A}},
  issn         = {{1949-2553}},
  keywords     = {{Bmi1; EphA7; neural stem cells; DNA methylation}},
  language     = {{eng}},
  month        = {{09}},
  number       = {{36}},
  pages        = {{58203--58217}},
  publisher    = {{Impact Journals}},
  series       = {{Oncotarget}},
  title        = {{The putative tumor suppressor gene EphA7 is a novel BMI-1 target}},
  url          = {{http://dx.doi.org/10.18632/oncotarget.11279}},
  doi          = {{10.18632/oncotarget.11279}},
  volume       = {{7}},
  year         = {{2016}},
}