Journal
TRENDS IN NEUROSCIENCES
Volume 32, Issue 11, Pages 559-565Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2009.07.005
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Funding
- National Institute on Aging Intramural Research Program
- Childhood Brain Tumor Foundation
- Pediatric Brain Tumor Foundation of the United States
- Accelerate Brain Cancer Cure
- Alexander and Margaret Stewart Trust
- Brain Tumor Society
- Goldhirsh Foundation
- Duke Comprehensive Cancer Center Stem Cell Initiative Grant
- NIH [NS047409, NS054276, CA116659]
- Damon Runyon Cancer Research Foundation
- Sidney Mmmel Foundation for Cancer Research Scholar
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Glioblastoma brain tumors harbor a small population of cancer stem cells that are resistant to conventional chemotherapeutic and radiation treatments, and are believed responsible for tumor recurrence and mortality. The identification of the epigenetic molecular mechanisms that control self-renewal of glioblastoma stem cells will foster development of targeted therapeutic approaches. The transcriptional repressor REST, best known for its role in controlling cell fate decisions in neural progenitor cells, may also be crucial for cancer stem cell self-renewal. Two novel mechanisms for regulating the stability of REST have recently been revealed: these involve the telomere-binding protein TRF2 and the ubiquitin E3 ligase SCF beta-TrCP. Reduced TRF2 binding to REST, and increased SCF beta-TrCP activity, target REST for proteasomal degradation and thereby inhibit cancer stem cell proliferation. Neurological side effects of treatments that target REST and TRF2 may be less severe than conventional brain tumor treatments because post-mitotic neurons do not express REST and have relatively stable telomeres.
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