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

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.
AuthorsJin Han, Shengtao Shi, Lan Min, Teresa Wu, Weiliang Xia, Weihai Ying
JournalNeurochemical research (Neurochem Res) Vol. 36 Issue 12 Pg. 2270-7 (Dec 2011) ISSN: 1573-6903 [Electronic] United States
PMID21833846 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Apoptosis Regulatory Proteins
  • Becn1 protein, mouse
  • MAP1LC3 protein, mouse
  • Microtubule-Associated Proteins
  • NAD
  • Niacinamide
  • Animals
  • Apoptosis Regulatory Proteins (biosynthesis)
  • Autophagy (drug effects)
  • Cell Survival (drug effects)
  • Mice
  • Microtubule-Associated Proteins (metabolism)
  • NAD (pharmacology)
  • Neuroblastoma
  • Niacinamide (pharmacology)
  • Oxidative Stress (drug effects)
  • Tumor Cells, Cultured

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