ArticleCancer research2009
Rapid DNA double-strand breaks resulting from processing of Cr-DNA cross-links by both MutS dimers.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 92 citations in OpenAlex.
- Do Ternary DNA-Cr(III)-Small Molecule Adducts Form?Biological trace element research · 2025Review
- Sensitive Detection of Histones and γ-H2AX by Immunoblotting: Problems and Solutions.Chemical research in toxicology · 2024Article
- Evolutionary origin of germline pathogenic variants in human DNA mismatch repair genes.Human genomics · 2024Article
- ATR activation by Cr-DNA damage is a major survival response establishing late S and G2 checkpoints after Cr(VI) exposure.Toxicology and applied pharmacology · 2023Article
- Examining the Potential Formation of Ternary DNA Complexes with Chromium‑Cysteine, Chromium-Ascorbate, and Chromium-Glutathione and Implications for Their Carcinogenicity.Biological trace element research · 2023Article
- Chemical mechanisms of DNA damage by carcinogenic chromium(VI).Advances in pharmacology (San Diego, Calif.) · 2023Article
- The multiple de novo copy number variant (MdnCNV) phenomenon presents with peri-zygotic DNA mutational signatures and multilocus pathogenic variation.Genome medicine · 2022Article
- Hexavalent chromium promotes differential binding of CTCF to its cognate sites in Euchromatin.Epigenetics · 2021Article
- Hexavalent chromium disrupts chromatin architecture.Seminars in cancer biology · 2021Review
- Comparative Study of Cytotoxicity, DNA Damage and Oxidative Stress Induced by Heavy Metals Cd(II), Hg(II) and Cr(III) in Yeast.Current microbiology · 2021Article
- Review
- Alpha lipoic acid antagonizes cytotoxicity of cobalt nanoparticles by inhibiting ferroptosis-like cell death.Journal of nanobiotechnology · 2020Article
- Vitamin C as a Modulator of the Response to Cancer Therapy.Molecules (Basel, Switzerland) · 2019Review
- Toxicological Antagonism among Welding Fume Metals: Inactivation of Soluble Cr(VI) by Iron.Chemical research in toxicology · 2018Article
- Monoubiquitinated γ-H2AX: Abundant product and specific biomarker for non-apoptotic DNA double-strand breaks.Toxicology and applied pharmacology · 2018Article
- Quinic acid and hypervalent chromium: a spectroscopic and kinetic study.RSC advances · 2018Article
- Tdp1 processes chromate-induced single-strand DNA breaks that collapse replication forks.PLoS genetics · 2018Article
- Systemic and local toxicity of metal debris released from hip prostheses: A review of experimental approaches.Nanomedicine : nanotechnology, biology, and medicine · 2018Review
- DNA mismatch repair protein Mlh1 is required for tetravalent chromium intermediate-induced DNA damage.Oncotarget · 2017Article
- Variation in Extracellular Detoxification Is a Link to Different Carcinogenicity among Chromates in Rodent and Human Lungs.Chemical research in toxicology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mismatch repair (MMR) strongly enhances cyto- and genotoxicity of several chemotherapeutic agents and environmental carcinogens. DNA double-strand breaks (DSB) formed after two replication cycles play a major role in MMR-dependent cell death by DNA alkylating drugs. Here, we examined DNA damage detection and the mechanisms of the unusually rapid induction of DSB by MMR proteins in response to carcinogenic chromium(VI). We found that MSH2-MSH6 (MutSalpha) dimer effectively bound DNA probes containing ascorbate-Cr-DNA and cysteine-Cr-DNA cross-links. Binary Cr-DNA adducts, the most abundant form of Cr-DNA damage, were poor substrates for MSH2-MSH6, and their toxicity in cells was weak and MMR independent. Although not involved in the initial recognition of Cr-DNA damage, MSH2-MSH3 (MutSbeta) complex was essential for the induction of DSB, micronuclei, and apoptosis in human cells by chromate. In situ fractionation of Cr-treated cells revealed MSH6 and MSH3 chromatin foci that originated in late S phase and did not require replication of damaged DNA. Formation of MSH3 foci was MSH6 and MLH1 dependent, whereas MSH6 foci were unaffected by MSH3 status. DSB production was associated with progression of cells from S into G(2) phase and was completely blocked by the DNA synthesis inhibitor aphidicolin. Interestingly, chromosome 3 transfer into MSH3-null HCT116 cells activated an alternative, MSH3-like activity that restored dinucleotide repeat stability and sensitivity to chromate. Thus, sequential recruitment and unprecedented cooperation of MutSalpha and MutSbeta branches of MMR in processing of Cr-DNA cross-links is the main cause of DSB and chromosomal breakage at low and moderate Cr(VI) doses.
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Registered trials
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