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Druggable binding sites in the multicomponent assemblies that characterise DNA double-strand-break repair through

Antonia Kefala Stavridi1, Robert Appleby1, Shikang Liang1

  • 1Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB21GA, Cambridgeshire, U.K.

Essays in Biochemistry
|June 25, 2020
PubMed

Insights

Non-homologous end joining (NHEJ) repairs DNA double-strand breaks. Targeting NHEJ components offers potential cancer therapies, especially by modulating protein-protein interactions, overcoming limitations of earlier drug development approaches.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Drug Discovery

Background:

  • Non-homologous end joining (NHEJ) is a critical DNA repair pathway for double-strand breaks.
  • Dysregulation of NHEJ components is implicated in cancer development and treatment resistance.

Purpose of the Study:

  • To review the role of NHEJ in cancer and its therapeutic potential.
  • To explore novel strategies for targeting NHEJ, focusing on protein-protein interactions.

Main Methods:

  • Review of existing literature on NHEJ pathways and cancer therapy.
  • Discussion of computational and structural biology advancements.
  • Analysis of protein-protein interaction inhibitor strategies.

Main Results:

  • NHEJ deregulation contributes to carcinogenesis and therapy resistance.
  • Targeting NHEJ offers a promising avenue for cancer treatment.
  • Modulating protein-protein interactions presents a novel approach to inhibit NHEJ complex assembly.

Conclusions:

  • Pharmacological targeting of NHEJ components, particularly via protein-protein interactions, is a viable strategy for cancer therapy.
  • Advances in computational biology enable exploration of new therapeutic targets within NHEJ pathways.
Keywords:
DNA-repairmulticomponent systemsstructural biologytherapeutics

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