Role of IL-6-mediated expression of NS5ATP9 in autophagy of liver cancer cells.

Abstract

This study aimed to investigate the relationship between interleukin-6 (IL-6) and NS5ATP9 in autophagy of liver cancer cells. Autophagy is one of the important regulators of the replication of hepatitis C virus and the survival of tumors. IL-6 is a multifunctional cytokine that plays an important role in autophagy and development of many kinds of tumors. However, the role of IL-6 in autophagy has not been fully explored. A previous study had shown that a novel gene, NS5ATP9, could modulate autophagy. The present study demonstrated that human IL-6 recombinant protein induced autophagy of HepG2 cells. Conversely, autophagy decreased after IL-6 was silenced or neutralized with monoclonal antibody against human IL-6. In addition, NS5ATP9 was upregulated by IL-6 via nuclear factor-kappaB activation, as detected by Western blot. Further studies indicated that the induction of autophagy by IL-6 could be attenuated by silencing NS5ATP9. Interestingly, the expression of NS5ATP9, in turn, resulted in the upregulation of IL-6. In conclusion, IL-6 could induce autophagy by expressing NS5ATP9, while NS5ATP9 upregulated IL-6 levels in turn, which further induced autophagy.

• Authors: Hongping Lu, Ming Han, Xiaoxue Yuan, Kelbinur Tursun, Yu Zhang, Yaru Li, Zhongshu Li, Shenghu Feng, Li Zhou, Zhipeng Pan, Qi Wang, Kai Han, Shunai Liu, Jun Cheng
• Journal: Journal of cellular physiology (J Cell Physiol) Vol. 233 Issue 12 Pg. 9312-9319 (12 2018) ISSN: 1097-4652 [Electronic] United States
• PMID: 29227529 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2017 Wiley Periodicals, Inc.

Chemical References

• Beclin-1
• DNA-Binding Proteins
• Interleukin-6
• MAP1LC3B protein, human
• Microtubule-Associated Proteins
• NF-kappa B
• PCLAF protein, human
• Recombinant Proteins

Topics

• Autophagy (drug effects, genetics)
• Beclin-1 (metabolism)
• DNA-Binding Proteins (genetics, metabolism)
• Gene Expression Regulation, Neoplastic (drug effects)
• Gene Knockdown Techniques
• Gene Silencing (drug effects)
• Hep G2 Cells
• Humans
• Interleukin-6 (metabolism)
• Liver Neoplasms (genetics, pathology)
• Microtubule-Associated Proteins (metabolism)
• NF-kappa B (metabolism)
• Neutralization Tests
• Recombinant Proteins (pharmacology)
• Up-Regulation (drug effects, genetics)