Inflammation and cancer: interweaving microRNA, free radical, cytokine and p53 pathways

被引:593
作者
Schetter, Aaron J. [1 ]
Heegaard, Niels H. H. [1 ,2 ]
Harris, Curtis C. [1 ]
机构
[1] NCI, Human Carcinogenesis Lab, Ctr Canc Res, NIH, Bethesda, MD 20892 USA
[2] Statens Serum Inst, Dept Clin Biochem & Immunol, DK-2300 Copenhagen, Denmark
基金
美国国家卫生研究院;
关键词
NF-KAPPA-B; CELL LUNG-CANCER; HELICOBACTER-PYLORI INFECTION; CHRONIC LYMPHOCYTIC-LEUKEMIA; PREVENT COLORECTAL ADENOMAS; OXIDE SYNTHASE EXPRESSION; COLITIS-ASSOCIATED CANCER; TUMOR-SUPPRESSOR GENE; HUMAN BREAST-CANCER; NITRIC-OXIDE;
D O I
10.1093/carcin/bgp272
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Chronic inflammation and infection are major causes of cancer. There are continued improvements to our understanding of the molecular connections between inflammation and cancer. Key mediators of inflammation-induced cancer include nuclear factor kappa B, reactive oxygen and nitrogen species, inflammatory cytokines, prostaglandins and specific microRNAs. The collective activity of these mediators is largely responsible for either a pro-tumorigenic or anti-tumorigenic inflammatory response through changes in cell proliferation, cell death, cellular senescence, DNA mutation rates, DNA methylation and angiogenesis. As our understanding grows, inflammatory mediators will provide opportunities to develop novel diagnostic and therapeutic strategies. In this review, we provide a general overview of the connection between inflammation, microRNAs and cancer and highlight how our improved understanding of these connections may provide novel preventive, diagnostic and therapeutic strategies to reduce the health burden of cancer.
引用
收藏
页码:37 / 49
页数:13
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