AI Article Synopsis
- The cMyc-driven group 3 (G3) medulloblastoma tumors are the most aggressive and often overexpress EZH2, which is linked to various roles in cancer.
- Deleting EZH2 in these tumors speeds up tumor growth, while re-expressing it can slow the progression by modifying histones.
- Gfi1, a proto-oncogene that EZH2 suppresses, can either enhance or counteract tumor growth depending on its expression level and interactions with other genes.
Article Abstract
The most aggressive of four medulloblastoma (MB) subgroups are cMyc-driven group 3 (G3) tumors, some of which overexpress EZH2, the histone H3K27 mono-, di-, and trimethylase of polycomb-repressive complex 2. Ezh2 has a context-dependent role in different cancers as an oncogene or tumor suppressor and retards tumor progression in a mouse model of G3 MB. Engineered deletions of Ezh2 in G3 MBs by gene editing nucleases accelerated tumorigenesis, whereas Ezh2 re-expression reversed attendant histone modifications and slowed tumor progression. Candidate oncogenic drivers suppressed by Ezh2 included Gfi1, a proto-oncogene frequently activated in human G3 MBs. Gfi1 disruption antagonized the tumor-promoting effects of Ezh2 loss; conversely, Gfi1 overexpression collaborated with Myc to bypass effects of Trp53 inactivation in driving MB progression in primary cerebellar neuronal progenitors. Although negative regulation of Gfi1 by Ezh2 may restrain MB development, Gfi1 activation can bypass these effects.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5415387 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2017.02.073 | DOI Listing |
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