Tumor Necrosis Factor (TNF) and Chemokines in Colitis-Associated Cancer

Cancers

Naofumi Mukaida¹  So-ichiro Sasakki¹ 

[1] Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, Kakuma-machi, Kanazawa 920-1192, Japan; E-Mail:

关键词: cyclooxygenase 2;    tumor-associated macrophage;    neovascularization;    NF-κB;    hypoxia inducible factor;   

DOI  :  10.3390/cancers3032811

来源: mdpi

【 摘 要 】

The connection between inflammation and tumorigenesis has been well established, based on a great deal of supporting evidence obtained from epidemiological, pharmacological, and genetic studies. One representative example is inflammatory bowel disease, because it is an important risk factor for the development of colon cancer. Moreover, intratumoral infiltration of inflammatory cells suggests the involvement of inflammatory responses also in other forms of sporadic as well as heritable colon cancer. Inflammatory responses and tumorigenesis activate similar sets of transcription factors such as NF-κB, Stat3, and hypoxia inducible factor and eventually enhances the expression of inflammatory cytokines including tumor necrosis factor (TNF) and chemokines. The expression of TNF and chemokines is aberrantly expressed in a mouse model of colitis-associated carcinogenesis as well as in inflammatory bowel disease and colon cancer in humans. Here, after summarizing the presumed actions of TNF and chemokines in tumor biology, we will discuss the potential roles of TNF and chemokines in chronic inflammation-associated colon cancer in mice.

【 授权许可】

CC BY   
© 2011 by the authors; licensee MDPI, Basel, Switzerland.