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 EphA7 inactivation via H3K27 trimethylation and DNA methylation.
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Prost, G., Braun, S., Hertwig, F., Winkler, M., Jagemann, L., Nolbrant, S., … Nuber, U. A. (2016). The putative tumor suppressor gene EphA7 is a novel BMI-1 target. Oncotarget, 7(36), 58203–58217. https://doi.org/10.18632/oncotarget.11279
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