NAD+ treatment induces delayed autophagy in Neuro2a cells partially by increasing oxidative stress

Neurochem Res. 2011 Dec;36(12):2270-7. doi: 10.1007/s11064-011-0551-x. Epub 2011 Aug 11.

Abstract

NAD(+) plays important roles in various biological processes. In this study, we reported that treatment of NAD(+) induces delayed autophagy in Neuro2a cells. Moreover, the effects of NAD(+) on the autophagy in the cells appear to be, at least partially, mediated by oxidative stress. However, nicotinamide, a degradation product of NAD(+), does not affect the autophagy. Our experiments have further indicated that the NAD(+)-induced autophagy contributes to the NAD(+)-induced decrease in the survival of these cells. In summary, our study has provided the first evidence that NAD(+) treatment induces autophagy in cancer cells such as Neuro2a cells, which contributes to the NAD(+)-induced decrease in cancer cell survival.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis Regulatory Proteins / biosynthesis
  • Autophagy / drug effects*
  • Beclin-1
  • Cell Survival / drug effects
  • Mice
  • Microtubule-Associated Proteins / metabolism
  • NAD / pharmacology*
  • Neuroblastoma
  • Niacinamide / pharmacology
  • Oxidative Stress / drug effects*
  • Tumor Cells, Cultured

Substances

  • Apoptosis Regulatory Proteins
  • Beclin-1
  • Becn1 protein, mouse
  • Map1lc3b protein, mouse
  • Microtubule-Associated Proteins
  • NAD
  • Niacinamide