AI Article Synopsis
- - Bmi1 is a gene linked to mouse lymphoma development that prevents cell death caused by the MYC gene by repressing the tumor suppressor genes Ink4a and Arf.
- - It encodes the BMI-1 protein, which primarily functions as a transcriptional repressor through modifying chromatin, impacting various genomic regions.
- - The study identifies EphA7, a possible tumor suppressor, as a direct target of BMI-1 in neural cells and lymphocytes, indicating that BMI1 overexpression may inactivate EphA7 through specific chemical modifications in the DNA.
Article 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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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295425 | PMC |
| http://dx.doi.org/10.18632/oncotarget.11279 | DOI Listing |
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