The receptor RAGE: Bridging inflammation and cancer
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BioMed Central
Open Access
Review
The receptor RAGE: Bridging inflammation and cancer Astrid Riehl, Julia Németh, Peter Angel* and Jochen Hess Address: German Cancer Research Center, DKFZ-ZMBH Alliance, Division of Signal Transduction and Growth Control (A100), Im Neuenheimer Feld 280, 69120 Heidelberg, Germany Email: Astrid Riehl - [email protected]; Julia Németh - [email protected]; Peter Angel* - [email protected]; Jochen Hess - [email protected] * Corresponding author
Published: 8 May 2009 Cell Communication and Signaling 2009, 7:12
doi:10.1186/1478-811X-7-12
Received: 17 February 2009 Accepted: 8 May 2009
This article is available from: http://www.biosignaling.com/content/7/1/12 © 2009 Riehl et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract The receptor for advanced glycation end products (RAGE) is a single transmembrane receptor of the immunoglobulin superfamily that is mainly expressed on immune cells, neurons, activated endothelial and vascular smooth muscle cells, bone forming cells, and a variety of cancer cells. RAGE is a multifunctional receptor that binds a broad repertoire of ligands and mediates responses to cell damage and stress conditions. It activates programs responsible for acute and chronic inflammation, and is implicated in a number of pathological diseases, including diabetic complications, stroke, atheriosclerosis, arthritis, and neurodegenerative disorders. The availability of Rage knockout mice has not only advanced our knowledge on signalling pathways within these pathophysiological conditions, but also on the functional importance of the receptor in processes of cancer. Here, we will summarize molecular mechanisms through which RAGE signalling contributes to the establishment of a pro-tumourigenic microenvironment. Moreover, we will review recent findings that provide genetic evidence for an important role of RAGE in bridging inflammation and cancer.
Introduction Numerous findings, ranging from epidemiological studies to molecular analyses of mouse models, have highlighted a strong contribution of chronic inflammation to tumour development [1,2]. Irrespective of the cause of cancerrelated inflammation, either driven by genetic alterations, tissue damage or arising from preceding infection, the generation of an inflammatory microenvironment supports tumourigenesis by promoting cancer cell survival, proliferation, migration, and invasion [3,4]. The generation of the pro-tumourigenic microenvironment strongly depends on the activation of several transcription factors, mainly nuclear factor-κB (NF-κB), signal transducer and activator of transcription 3 (Stat3) and hypoxia-inducible
factor-1α (HIF-1α) [4]. These transcription factors regulate the expression of important cytokines, su
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