Secretion of one adipokine Nampt/Visfatin suppresses the inflammatory stress-induced NF-κB activity and affects Nampt-dependent cell viability in Huh-7 cells.

ABSTRACT: Nampt/visfatin acts in both intracellular and extracellular compartments to regulate multiple biological roles, including NAD metabolism, cancer, inflammation, and senescence. However, its function in chronic inflammation and carcinogenesis in hepatocellular carcinoma (HCC) has not been well-defined. Here we use Huh-7 hepatoma cells as a model to determine how Nampt/visfatin affects cellular survival under oxidative stress. We found that the transition of Nampt/visfatin from intracellular into extracellular form was induced by H2O2 treatment in 293T cells and confirmed that this phenomenon was not due to cell death but through the secretion of Nampt/visfatin. In addition, Nampt/visfatin suppressed cell viability in oxidative treatment in Huh-7 cells and acted on the inhibition of hepatoma

SUBMITTER: Lin YC 

PROVIDER: S-EPMC4357042 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature