ArticleInternational journal of molecular sciences2017
Dihydrocoumarin, an HDAC Inhibitor, Increases DNA Damage Sensitivity by Inhibiting Rad52.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 21 citations in OpenAlex.
- R-Loop-Mediated ssDNA Breaks Accumulate Following Short-Term Exposure to the HDAC Inhibitor Romidepsin.Molecular cancer research : MCR · 2021Article
- Yeast Rpn4 Links the Proteasome and DNA Repair viaInternational journal of molecular sciences · 2020Article
- Class I histone deacetylase inhibition is synthetic lethal with BRCA1 deficiency in breast cancer cells.Acta pharmaceutica Sinica. B · 2020Article
- Hydroxygenkwanin Inhibits Class I HDAC Expression and Synergistically Enhances the Antitumor Activity of Sorafenib in Liver Cancer Cells.Frontiers in oncology · 2020Article
- In Search of Panacea-Review of Recent Studies Concerning Nature-Derived Anticancer Agents.Nutrients · 2019Review
- The Process and Strategy for Developing Selective Histone Deacetylase 3 Inhibitors.Molecules (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Effective DNA repair enables cancer cells to survive DNA damage induced by chemotherapeutic or radiotherapeutic treatments. Therefore, inhibiting DNA repair pathways is a promising therapeutic strategy for increasing the efficacy of such treatments. In this study, we found that dihydrocoumarin (DHC), a flavoring agent, causes deficiencies in double-stand break (DSB) repair and prolonged DNA damage checkpoint recovery in yeast. Following DNA damage, Rad52 recombinase was revealed to be inhibited by DHC, which results in deficiencies in DSB repair and prolonged DNA damage checkpoint recovery. The deletion of
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Registered trials
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