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Author Spotlight: Developing Novel Anticancer Therapeutics Targeting the DNA Damage Response
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Author Spotlight: Developing Novel Anticancer Therapeutics Targeting the DNA Damage Response

Published on: June 14, 2024

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DNA double-strand break formation and repair as targets for novel antibiotic combination chemotherapy

Vincent Amarh1, Patrick K Arthur1

  • 1Department of Biochemistry, Cell & Molecular Biology, West African Center for Cell Biology of Infectious Pathogens, University of Ghana, PO Box LG54, Legon, Accra, Ghana.

Future Science OA
|September 20, 2019
PubMed

Insights

Persistent DNA double-strand breaks (DSBs) are lethal to bacteria. This study explores novel strategies to combat antibiotic resistance by targeting bacterial DSB repair pathways and developing new DSB-inducing compounds.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Drug Discovery

Background:

  • Unrepaired DNA double-strand breaks (DSBs) are lethal to bacterial cells.
  • Current antibiotics inducing DSBs face resistance due to recurrent usage.
  • Existing literature covers bacterial drug resistance mechanisms and drug discovery approaches.

Purpose of the Study:

  • To propose a hypothetical chemotherapeutic strategy to minimize resistance to novel DSB-inducing compounds.
  • To explore bacterial DSB repair pathways as potential targets for new antibiotic development.

Main Methods:

  • Focus on theoretical chemotherapeutic strategies.
  • Highlighting potential therapeutic targets within bacterial DSB repair mechanisms.

Main Results:

  • A hypothetical strategy for minimizing resistance to DSB-inducing agents is presented.
  • Bacterial DSB repair pathways are identified as promising targets for novel antibiotic discovery.

Conclusions:

  • Targeting bacterial DSB repair pathways offers a novel avenue for antibiotic development.
  • Minimizing resistance to DSB-inducing drugs is crucial for effective bacterial infection treatment.
Keywords:
DNA double-strand breakSOS responseantibiotic combination chemotherapycell-based assaysgenome stabilityhomologous recombinationnonhomologous end joiningquinolone resistanceribosome inhibitorstype II topoisomerase

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