Nucleases in homologous recombination as targets for cancer therapy
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
24928444
DOI
10.1016/j.febslet.2014.06.010
PII: S0014-5793(14)00464-5
Knihovny.cz E-resources
- Keywords
- Cancer therapy, Genomic integrity, Homologous recombination, Inhibitor, Nuclease,
- MeSH
- Molecular Targeted Therapy MeSH
- Deoxyribonucleases antagonists & inhibitors genetics metabolism MeSH
- DNA Repair Enzymes antagonists & inhibitors genetics metabolism MeSH
- Homologous Recombination * MeSH
- Enzyme Inhibitors pharmacology therapeutic use MeSH
- Humans MeSH
- Neoplasms drug therapy enzymology genetics MeSH
- Recombinational DNA Repair * MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Deoxyribonucleases MeSH
- DNA Repair Enzymes MeSH
- Enzyme Inhibitors MeSH
Genomic DNA is constantly challenged from endogenous as well as exogenous sources. The DNA damage response (DDR) mechanism has evolved to combat these challenges and ensure genomic integrity. In this review, we will focus on repair of DNA double-strand breaks (DSB) by homologous recombination and the role of several nucleases and other recombination factors as suitable targets for cancer therapy. Their inactivation as well as overexpression have been shown to sensitize cancer cells by increasing toxicity to DNA-damaging agents and radiation or to be responsible for resistance of cancer cells. These factors can also be used in targeted cancer therapy by taking advantage of specific genetic abnormalities of cancer cells that are not present in normal cells and that result in cancer cell lethality.
References provided by Crossref.org
MUS81 cleaves TOP1-derived lesions and other DNA-protein cross-links
Esc2 promotes Mus81 complex-activity via its SUMO-like and DNA binding domains
