The putative tumor suppressor gene EphA7 is a novel BMI-1 target
(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.
(Less)
- author
- organization
-
- Stem Cell Center
- Division of Translational Cancer Research
- Developmental and Regenerative Neurobiology (research group)
- Division of Molecular Medicine and Gene Therapy
- Stem Cell Metabolism (research group)
- Division of Molecular Hematology (DMH)
- StemTherapy: National Initiative on Stem Cells for Regenerative Therapy
- publishing date
- 2016-09-06
- 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
- 2024-04-14 12:26:43
@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}}, }