Journal
ONCOTARGET
Volume 7, Issue 36, Pages 58203-58217Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.11279
Keywords
Bmi1; EphA7; neural stem cells; DNA methylation
Categories
Funding
- Swedish Research Council (Vetenskapsradet) [VR521-2010-4508]
- Swedish Cancer Society (Cancerfonden) [CAN2012/588]
- Swedish Childhood Cancer Society (Barncancerfonden) [BCF12/2007]
- AFA insurance [AFA120261]
- StemTherapy
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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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