[1]李杰,闫堃,杨屹,等.白介素-17通过拮抗γ-干扰素的作用促进小鼠肝癌细胞的生长与增殖[J].南方医科大学学报,2019,(01):1.[doi:10.12122/j.issn.1673-4254.2019.01.01]
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白介素-17通过拮抗γ-干扰素的作用促进小鼠肝癌细胞的生长与增殖()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2019年01期
页码:
1
栏目:
出版日期:
2019-01-26

文章信息/Info

Title:
Interleukin-17 promotes mouse hepatoma cell proliferation by antagonizing interferon-γ
作者:
李杰闫堃杨屹李华王志东徐心
关键词:
白介素-17干扰素-γ原发性肝癌
Keywords:
interleukin-17 interferon-γ hepatocellular carcinoma
DOI:
10.12122/j.issn.1673-4254.2019.01.01
摘要:
目的探讨白介素(IL-17)与γ-干扰素(IFN-γ)的相互作用对小鼠肝癌细胞Hepa1-6 生长的影响。方法IL-17 单独或与 IFN-γ联合干预小鼠Hepa1-6细胞,采用MTT法检测细胞增殖情况,流式细胞仪检测细胞周期分布情况,Western blot检测细胞 增殖相关蛋白PCNA、Cyclin D1、P21及P16的表达,以及胞内信号分子p38MAPK、ERK1/2和Stat1的磷酸化水平。结果IFN-γ 可显著抑制Hepa1-6细胞的生长,明显增加细胞G0/G1期的比例,同时减少PCNA和Cyclin D1蛋白,并增加P21蛋白的表达。 IL-17单独应用不影响Hepa1-6细胞的生长,但它可显著拮抗IFN-γ的作用。与IFN-γ单独处理组相比,IL-17与IFN-γ联用可以显 著降低细胞G0/G1期的比例;明显增加PCNA和Cyclin D1,同时降低P21蛋白的表达。IL-17不影响细胞Stat1的磷酸化水平, 但可以抑制IFN-γ所引发的p38MAPK及ERK1/2的磷酸化。结论IL-17可与IFN-γ的作用相拮抗从而显著促进肝癌细胞的生长。
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. Conclusion 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.

相似文献/References:

[1]李朝旭,唐际存,叶招明.IFN-γ增强人γδT细胞杀伤骨肉瘤细胞的研究[J].南方医科大学学报,2013,(01):22.
[2]蒋娜,廖雯婷,匡希斌.大黄素对病毒性心肌炎小鼠IL-23/IL-17炎症轴、Th17细胞及病毒复制的影响[J].南方医科大学学报,2014,(03):373.

更新日期/Last Update: 1900-01-01