The DOI matches its Crossref record; 114 of the 114 references it cites were found in a registry or an index.
Tumor Cell Death Induced by Topoisomerase-Targeting Drugs
Abstract
DNA topoisomerases are double-edged swords. They are essential for many vital functions of DNA during normal cell growth. However, they are also highly vulnerable under various physiological and nonphysiological stresses because of their delicate act on breaking and rejoining DNA. These stresses (e.g. exposure to topoisomerase poisons, acidic pH, and oxidative stresses) can convert DNA topoisomerases into DNA-breaking nucleases, resulting in cell death and/or genomic instability. The importance of topoisomerase-mediated DNA cleavage in tumor cell death and carcinogenesis has been recognized. This review focuses on recent findings concerning the molecular mechanisms of the stress responses to topoisomerase-mediated DNA damage. The involvement of ubiquitin/26S proteasome and SUMO/UBC9 in these processes, as well as the role of topoisomerase cleavable complexes in apoptotic cell death are discussed.
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Cites
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Ma, Y., & Hendershot, L. M. (2004) · Nature Reviews Cancer · doi:10.1038/nrc1505 · Cited by 710
The DNA cleavage reaction of topoisomerase II: wolf in sheep's clothing
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DNA topoisomerase II, genotoxicity, and cancer
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Topoisomerase I-Mediated Inhibition of Hypoxia-Inducible Factor 1
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Central role of mitochondria in drug-induced liver injury
Pessayre, D., Fromenty, B., Berson, A., Robin, M.-A., Lettéron, P., Moreau, R., & Mansouri, A. (2012) · Drug Metabolism Reviews · doi:10.3109/03602532.2011.604086 · Cited by 277
Metadata
- Authors
- Li, T.-K., & Liu, L. F.
- Venue
- Annual Review of Pharmacology and Toxicology
- Publisher
- Annual Reviews
- Published
- 2001-04
- Volume
- 41
- Issue
- 1
- Pages
- 53-77
- ISSN
- 0362-1642 (ISSN-L)
- 1545-4304
- OpenAlex
- W2160948762
- Cited by
- 508
- References
- 114
- FWCI
- 1.78
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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