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J Cell Physiol. 2018 Dec;233(12):9312-9319. doi: 10.1002/jcp.26343. Epub 2018 Jun 26.

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

Lu H1,2, Han M1,2,3, Yuan X1,2, Tursun K2,4, Zhang Y1,2, Li Y1,2, Li Z1,2, Feng S2,3, Zhou L2,3, Pan Z2,5, Wang Q1,2, Han K1,2, Liu S1,2, Cheng J1,2,3.

Author information

1
Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, China.
2
Beijing Key Laboratory of Emerging Infectious Diseases, Beijing, China.
3
Peking University Ditan Teaching Hospital, Beijing, China.
4
The First Affiliated Hospital of Xinjiang Medical University, Xinjiang, China.
5
Dalian University, Dalian, China.

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.

KEYWORDS:

IL-6; NS5ATP9; autophagy; hepatocellular carcinoma; microenvironment

PMID:
29227529
DOI:
10.1002/jcp.26343

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