Secretion of one adipokine Nampt/visfatin suppresses the inflammatory stress-induced NF- B activity and affects Nampt-dependent cell viability in huh-7 cells

Yi Ching Lin, Hui Chung Wu, Chen Chung Liao, Yi Chih Chou, Shwu Fen Pan, Chi Ming Chiu*

*此作品的通信作者

研究成果: Article同行評審

16 引文 斯高帕斯(Scopus)

摘要

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 Htreatment 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 cell growth. Oxidative stress also reduced the Nampt-mediated activation of NF-B gene expression. In this study, we identify a novel feature of Nampt/visfatin which functions as an adipokine that can be secreted upon cellular stress. Our results provide an example to understand how adipokine interacts with chemotherapeutic treatment by oxidative stress in HCC.

原文English
文章編號392471
期刊Mediators of Inflammation
2015
DOIs
出版狀態Published - 26 2月 2015

指紋

深入研究「Secretion of one adipokine Nampt/visfatin suppresses the inflammatory stress-induced NF- B activity and affects Nampt-dependent cell viability in huh-7 cells」主題。共同形成了獨特的指紋。

引用此