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

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.

• Authors: Jin Han, Shengtao Shi, Lan Min, Teresa Wu, Weiliang Xia, Weihai Ying
• Journal: Neurochemical research (Neurochem Res) Vol. 36 Issue 12 Pg. 2270-7 (Dec 2011) ISSN: 1573-6903 [Electronic] United States
• PMID: 21833846 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

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

Topics

• 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