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Nampt is involved in DNA double-strand break repair

Bingtao Zhu1, Xiaoli Deng, Yifan Sun

  • 1Beijing Key Laboratory of DNA Damage Response, College of Life Science, Capital Normal University, Beijing 100048, P. R. China.

Chinese Journal of Cancer
|June 19, 2012
PubMed

Insights

Nicotinamide phosphoribosyltransferase (Nampt) suppresses homologous recombination (HR) DNA repair while enhancing non-homologous end joining (NHEJ) repair. Inhibiting Nampt delays cellular senescence and promotes proliferation in normal and cancer cells.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • DNA double-strand breaks (DSBs) are severe DNA damage, repaired by homologous recombination (HR) or non-homologous end joining (NHEJ).
  • Genomic instability from DNA damage response defects increases cancer risk.
  • Nicotinamide phosphoribosyltransferase (Nampt), involved in NAD+ metabolism, is upregulated in various tumors.

Purpose of the Study:

  • To investigate the role of Nampt in DNA double-strand break repair pathways.
  • To determine the effect of Nampt on homologous recombination and non-homologous end joining.
  • To assess the impact of Nampt on cellular senescence and proliferation.

Main Methods:

  • Small interfering RNA (siRNA) was used to deplete Nampt expression.
  • Physical association of Nampt with key HR (CtIP) and NHEJ (DNA-PKcs/Ku80) factors was examined.
  • DSB repair efficiency, cell proliferation, and senescence (β-galactosidase staining) were assessed.

Main Results:

  • Nampt physically interacts with CtIP (HR) and DNA-PKcs/Ku80 (NHEJ) components.
  • Nampt depletion resulted in impaired NHEJ-mediated DSB repair and enhanced HR-mediated repair.
  • Inhibition of Nampt promoted proliferation in cancer cells and normal fibroblasts and delayed senescence in normal fibroblasts.

Conclusions:

  • Nampt acts as a suppressor of HR-mediated DSB repair.
  • Nampt enhances NHEJ-mediated DSB repair.
  • Nampt contributes to the acceleration of cellular senescence.

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