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BMI1 Confers Radioresistance to Normal and Cancerous Neural Stem Cells through Recruitment of the DNA Damage Response Machinery
Abstract
Glioblastoma multiforme (GBM) is an aggressive brain tumor that is resistant to all known therapies. Within these tumors, a CD133-positive cancer-initiating neural stem cell (NSC) population was shown to be resistant to gamma radiation through preferential activation of the DNA double-strand break (DSB) response machinery, including the ataxia-telangiectasia-mutated (ATM) kinase. The polycomb group protein BMI1 is enriched in CD133-positive GBM cells and required for their self-renewal in an INK4A/ARF-independent manner through transcriptional repression of alternate tumor suppressor pathways. We report here that BMI1 copurifies with DNA DSB response and nonhomologous end joining (NHEJ) repair proteins in GBM cells. BMI1 was enriched at the chromatin after irradiation and colocalized and copurified with ATM and the histone γH2AX. BMI1 also preferentially copurified with NHEJ proteins DNA-PK, PARP-1, hnRNP U, and histone H1 in CD133-positive GBM cells. BMI1 deficiency in GBM cells severely impaired DNA DSB response, resulting in increased sensitivity to radiation. In turn, BMI1 overexpression in normal NSCs enhanced ATM recruitment to the chromatin, the rate of γH2AX foci resolution, and resistance to radiation. BMI1 thus displays a previously uncharacterized function in controlling DNA DSB response and repair. Pharmacological inhibition of BMI1 combined with radiation therapy may provide an effective mean to target GBM stem cells.
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Activation of PRCs, evident from increased expression of BMI1 and SUZ12, contributes to radio-resistance of tumor cells, including glioblastoma.
“Thus, the activation of PRCs, evident from increased expression of BMI1 and SUZ12,77 contributed to the radio-resistance of tumor cells,137,138 including glioblastoma.139,140”
From MiR-128-3p – a gray eminence of the human central nervous system (2024) · cites this paper as [139]
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Bmi-1 is required for maintenance of adult self-renewing haematopoietic stem cells.
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“Importantly, most Bmi1 functions in development, stem cell maintenance, and cancer have been attributed to transcriptional repression of the Ink4a/Arf locus (Sherr, 2001; Sharpless et al., 2004; Valk-Lingbeek et al., 2004).”
BackgroundIrreversible chromosome damage accumulates rapidly in the absence of ATM kinase activity
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Metadata
- Authors
- Facchino, S., Abdouh, M., Chatoo, W., & Bernier, G.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2010-07-28
- Volume
- 30
- Issue
- 30
- Pages
- 10096-10111
- ISSN
- 0270-6474
- 1529-2401
- Cited by
- 253
- References
- 7
- Language
- en
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