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

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Carcinogenesis 2010 31(1):37-49; doi:10.1093/carcin/bgp272

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

pathways

J. Schetter1, Niels H. H. Heegaard1,2 and Curtis C. 1,*

1 Laboratory of Human Carcinogenesis, Center for Cancer Research, National

Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA

2 Department of Clinical Biochemistry and Immunology, Statens Serum Institute,

Copenhagen, DK-2300, Denmark

* To whom correspondence should be addressed. Tel: +1 301 496 2048; Fax: +1 301

496 0497; Email: harrisc@...

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.

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