ArticleCancer research2012
Targeting the transposase domain of the DNA repair component Metnase to enhance chemotherapy.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Targeting Replication Stress Response Pathways to Enhance Genotoxic Chemo- and Radiotherapy.Molecules (Basel, Switzerland) · 2022Review
- SETMAR, a case of primate co-opted genes: towards new perspectives.Mobile DNA · 2022Review
- Article
- Metnase and EEPD1: DNA Repair Functions and Potential Targets in Cancer Therapy.Frontiers in oncology · 2022Review
- Structure, Activity, and Function of SETMAR Protein Lysine Methyltransferase.Life (Basel, Switzerland) · 2021Review
- Distinct roles of structure-specific endonucleases EEPD1 and Metnase in replication stress responses.NAR cancer · 2020Article
- HIV‑1 integrase inhibitors targeting various DDE transposases: Retroviral integration versus RAG‑mediated recombination (Review).Molecular medicine reports · 2019Review
- Ligand Screening Systems for Human Glucose Transporters as Tools in Drug Discovery.Frontiers in chemistry · 2018Review
- Enrofloxacin enhances the effects of chemotherapy in canine osteosarcoma cells with mutant and wild-type p53.Veterinary and comparative oncology · 2017Article
- SETMAR isoforms in glioblastoma: A matter of protein stability.Oncotarget · 2017Article
- Discovery of a specific inhibitor of human GLUT5 by virtual screening and in vitro transport evaluation.Scientific reports · 2016Article
- The SET Domain Is Essential for Metnase Functions in Replication Restart and the 5' End of SS-Overhang Cleavage.PloS one · 2015Article
- Inhibition of lung tumor growth by targeting EGFR/VEGFR-Akt/NF-κB pathways with novel theanine derivatives.Oncotarget · 2014Article
- Ciprofloxacin as a potential radio-sensitizer to tumor cells and a radio-protectant for normal cells: differential effects on γ-H2AX formation, p53 phosphorylation, Bcl-2 production, and cell death.Molecular and cellular biochemistry · 2014Article
- The DDN catalytic motif is required for Metnase functions in non-homologous end joining (NHEJ) repair and replication restart.The Journal of biological chemistry · 2014Article
- Structural basis of Mos1 transposase inhibition by the anti-retroviral drug Raltegravir.ACS chemical biology · 2014Article
- Potential role for the Metnase transposase fusion gene in colon cancer through the regulation of key genes.PloS one · 2014Article
- The DNA repair component Metnase regulates Chk1 stability.Cell division · 2014Article
- Customized chemotherapy in metastatic non-small cell lung cancer (NSCLC).Translational lung cancer research · 2013Review
- Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
Previous studies have shown that the DNA repair component Metnase (SETMAR) mediates resistance to DNA damaging cancer chemotherapy. Metnase has a nuclease domain that shares homology with the Transposase family. We therefore virtually screened the tertiary Metnase structure against the 550,000 compound ChemDiv library to identify small molecules that might dock in the active site of the transposase nuclease domain of Metnase. We identified eight compounds as possible Metnase inhibitors. Interestingly, among these candidate inhibitors were quinolone antibiotics and HIV integrase inhibitors, which share common structural features. Previous reports have described possible activity of quinolones as antineoplastic agents. Therefore, we chose the quinolone ciprofloxacin for further study, based on its wide clinical availability and low toxicity. We found that ciprofloxacin inhibits the ability of Metnase to cleave DNA and inhibits Metnase-dependent DNA repair. Ciprofloxacin on its own did not induce DNA damage, but it did reduce repair of chemotherapy-induced DNA damage. Ciprofloxacin increased the sensitivity of cancer cell lines and a xenograft tumor model to clinically relevant chemotherapy. These studies provide a mechanism for the previously postulated antineoplastic activity of quinolones, and suggest that ciprofloxacin might be a simple yet effective adjunct to cancer chemotherapy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.