The DOI matches its Crossref record; 27 of the 27 references it cites were found in a registry or an index.
Antitelomerase Therapy Provokes ALT and Mitochondrial Adaptive Mechanisms in Cancer
Open accessAbstract
SUMMARY To assess telomerase as a cancer therapeutic target and determine adaptive mechanisms to telomerase inhibition, we modeled telomerase reactivation and subsequent extinction in T-cell lymphomas arising in Atm-/- mice engineered with an inducible telomerase reverse transcriptase allele. Telomerase reactivation in the setting of telomere dysfunction enabled full malignant progression with alleviation of telomere dysfunction-induced checkpoints. These cancers possessed copy number alterations targeting key loci in human T-cell lymphomagenesis. Upon telomerase extinction, tumor growth eventually slowed with re-instatement of telomere dysfunction-induced checkpoints, yet growth subsequently resumed as tumors acquired Alternative Lengthening of Telomeres (ALT) and aberrant transcriptional networks centering on mitochondrial biology and oxidative defense. ALT+ tumors acquired amplification/overexpression of PGC-1β, a master regulator of mitochondrial biogenesis and function, and they showed marked sensitivity to PGC-1β or SOD2 knock-down. Genetic modeling of telomerase extinction reveals vulnerabilities that motivate coincidental inhibition of mitochondrial maintenance and oxidative defense mechanisms to enhance anti-telomerase cancer therapy.
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Cites
Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
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A DNA damage checkpoint response in telomere-initiated senescence
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Cited by
Telomeres: history, health, and hallmarks of aging
Chakravarti, D., LaBella, K. A., & DePinho, R. A. (2021) · Cell · doi:10.1016/j.cell.2020.12.028 · Cited by 637
Self-citationMitochondrial Dysfunction in Cancer
Boland, M. L., Chourasia, A. H., & Macleod, K. F. (2013) · Frontiers in Oncology · doi:10.3389/fonc.2013.00292 · Cited by 489
RNaseH1 regulates TERRA-telomeric DNA hybrids and telomere maintenance in ALT tumour cells
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Axis of ageing: telomeres, p53 and mitochondria
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Self-citationRapid induction of alternative lengthening of telomeres by depletion of the histone chaperone ASF1
O'Sullivan, R. J., Arnoult, N., Lackner, D. H., Oganesian, L., Haggblom, C., Corpet, A., Almouzni, G., & Karlseder, J. (2014) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.2754 · Cited by 259
Metadata
- Authors
- Hu, J., Hwang, S. S., Liesa, M., Gan, B., Sahin, E., Jaskelioff, M., Ding, Z., Ying, H., Boutin, A. T., Zhang, H., Johnson, S., Ivanova, E., Kost-Alimova, M., Protopopov, A., Wang, Y. A., Shirihai, O. S., Chin, L., & DePinho, R. A.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-02
- Volume
- 148
- Issue
- 4
- Pages
- 651-663
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2168203939
- Cited by
- 296
- References
- 27
- FWCI
- 18.30
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Hu, J., Hwang, S. S., Liesa, M., Gan, B., Sahin, E., Jaskelioff, M., Ding, Z., Ying, H., Boutin, A. T., Zhang, H., Johnson, S., Ivanova, E., Kost-Alimova, M., Protopopov, A., Wang, Y. A., Shirihai, O. S., Chin, L., & DePinho, R. A. (2012). Antitelomerase Therapy Provokes ALT and Mitochondrial Adaptive Mechanisms in Cancer. Cell. https://doi.org/10.1016/j.cell.2011.12.028
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