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学科主题临床医学
Macrophages promote benzopyrene-induced tumor transformation of human bronchial epithelial cells by activation of NF-kappa B and STAT3 signaling in a bionic airway chip culture and in animal models
Li, Encheng1; Xu, Zhiyun1; Zhao, Hui2; Sun, Zhao1; Wang, Lei3; Guo, Zhe1; Zhao, Yang1; Gao, Zhancheng4; Wang, Qi1
关键词Macrophages malignant transformation NF-kappa B STAT3 microfluidic chip
刊名ONCOTARGET
2015-04-20
6期:11页:8900-8913
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Cell Biology
资助者Natural Science Foundation of China ; Innovative Research Team in University of the Chinese Ministry of Education ; Natural Science Foundation of China ; Innovative Research Team in University of the Chinese Ministry of Education
研究领域[WOS]Oncology ; Cell Biology
关键词[WOS]LUNG-CANCER ; BREAST-CANCER ; INFLAMMATION ; EXPRESSION ; TISSUES
英文摘要

We investigated the role of macrophages in promoting benzopyrene (BaP)induced malignant transformation of human bronchial epithelial cells using a BaP-induced tumor transformation model with a bionic airway chip in vitro and in animal models. The bionic airway chip culture data showed that macrophages promoted BaP-induced malignant transformation of human bronchial epithelial cells, which was mediated by nuclear factor (NF)-kappa B and STAT3 pathways to induce cell proliferation, colony formation in chip culture, and tumorigenicity in nude mice. Blockage of interleukin (IL)-6 or tumor necrosis factor (TNF)-alpha signaling or inhibition of NF-kappa B, STAT3, or cyclinD1 expression abrogated the effect of macrophages on malignant transformation in the bionic airway chip culture. In vivo, macrophages promoted lung tumorigenesis in a carcinogen-induced animal model. Similarly, blockage of NF-kappa B, STAT3, or cyclinD1 using siRNA transfection decreased the carcinogen-induced tumorigenesis in rats. We demonstrated that macrophages are critical in promoting lung tumorigenesis and that the macrophage-initiated TNF-alpha/NF-kappa B/cyclinD1 and IL-6/STAT3/cyclinD1 pathways are primarily responsible for promoting lung tumorigenesis.

语种英语
所属项目编号91129733 ; 81330060 ; IRT13049
资助者Natural Science Foundation of China ; Innovative Research Team in University of the Chinese Ministry of Education ; Natural Science Foundation of China ; Innovative Research Team in University of the Chinese Ministry of Education
WOS记录号WOS:000358774600034
引用统计
被引频次:10[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/61748
专题北京大学第二临床医学院
作者单位1.Dalian Med Univ, Affiliated Hosp 2, Dept Resp Med, Dalian, Peoples R China
2.Dalian Med Univ, Affiliated Hosp 2, Dept Phys Examinat Ctr, Dalian, Peoples R China
3.Dalian Univ Technol, Liaoning Prov Key Lab Micro Nano Technol, Dalian, Peoples R China
4.Peking Univ, Peoples Hosp, Dept Resp & Crit Care Med, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Li, Encheng,Xu, Zhiyun,Zhao, Hui,et al. Macrophages promote benzopyrene-induced tumor transformation of human bronchial epithelial cells by activation of NF-kappa B and STAT3 signaling in a bionic airway chip culture and in animal models[J]. ONCOTARGET,2015,6(11):8900-8913.
APA Li, Encheng.,Xu, Zhiyun.,Zhao, Hui.,Sun, Zhao.,Wang, Lei.,...&Wang, Qi.(2015).Macrophages promote benzopyrene-induced tumor transformation of human bronchial epithelial cells by activation of NF-kappa B and STAT3 signaling in a bionic airway chip culture and in animal models.ONCOTARGET,6(11),8900-8913.
MLA Li, Encheng,et al."Macrophages promote benzopyrene-induced tumor transformation of human bronchial epithelial cells by activation of NF-kappa B and STAT3 signaling in a bionic airway chip culture and in animal models".ONCOTARGET 6.11(2015):8900-8913.
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