Interleukin-17 promotes mouse hepatoma cell proliferation by antagonizing interferon-γ.
10.12122/j.issn.1673-4254.2019.01.01
- Author:
Jie LI
1
;
Kun YAN
1
;
Yi YANG
1
;
Hua LI
1
;
Zhidong WANG
1
;
Xin XU
1
Author Information
1. Department of General Surgery, Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
- Publication Type:Journal Article
- Keywords:
hepatocellular carcinoma;
interferon-γ;
interleukin-17
- MeSH:
Animals;
Carcinoma, Hepatocellular;
metabolism;
pathology;
Cell Cycle;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Cyclin D1;
metabolism;
Cyclin-Dependent Kinase Inhibitor p21;
metabolism;
Interferon-gamma;
antagonists & inhibitors;
Interleukin-17;
pharmacology;
Liver Neoplasms;
metabolism;
pathology;
Mice;
Neoplasm Proteins;
metabolism;
Proliferating Cell Nuclear Antigen;
metabolism
- From:
Journal of Southern Medical University
2019;39(1):1-5
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the interaction between interleukin-17 (IL-17) and interferon-γ (IFN-γ) and how their interaction affects the growth of mouse hepatoma Hepa1-6 cells.
METHODS:Hepa1-6 cells treated with IL-17 and IFN-γ either alone or in combination were examined for changes in cell proliferation using MTT assay and in cell cycle distribution using flow cytometry. Western blotting was used to detect the protein expression levels of proliferating cell nuclear antigen (PCNA), cyclin D1, P21 and P16 and the phosphorylation of p38MAPK, ERK1/2 and Stat1 in the cells.
RESULTS:Compared with control group, IFN-γ treatment obviously inhibited the growth and proliferation of Hepa1-6 cells, induced cell cycle arrest at G0/G1 phase, reduced the protein expression of PCNA and cyclin D1, and increased the protein expression of P21. IL-17 alone had no effect on the growth of Hepa1-6 cells. In the combined treatment, IL-17 significantly antagonized the effects of IFN-γ. Compared with those treated with IFN-γ alone, the cells with the combined treatment showed significantly decreased G0/G1 cell population, increased the protein expressions of PCNA and cyclin D1, and decreased the protein expression of P21. IL-17 significantly inhibited IFN-γ-induced phosphorylation of p38MAPK and ERK1/2 without affecting the phosphorylation of Stat1.
CONCLUSIONS:IL-17 obviously reverses the antitumor effects of IFN-γ to promote the proliferation of mouse hepatoma cells and accelerate the development of hepatocellular carcinoma.
