| First Author | Prost G | Year | 2016 |
| Journal | Oncotarget | Volume | 7 |
| Issue | 36 | Pages | 58203-58217 |
| PubMed ID | 27533460 | Mgi Jnum | J:310740 |
| Mgi Id | MGI:6763818 | Doi | 10.18632/oncotarget.11279 |
| Citation | Prost G, et al. (2016) The putative tumor suppressor gene EphA7 is a novel BMI-1 target. Oncotarget 7(36):58203-58217 |
| abstractText | 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. |
