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JCI online ahead of print table of contents for March 18, 2014
Date:3/18/2014

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AUTHOR CONTACT: Glenn I Fishman
NYU School of Medicine, New York, NY, USA
Phone: 212-263-3967; Fax: 212-263-3972; E-mail: glenn.fishman@med.nyu.edu

View this article at: http://www.jci.org/articles/view/75240


Inflammatory feedback loop promotes colorectal cancer metastasis

Induction of the epithelial-mesenchymal transition (EMT) in cancer cells is associated with an increased capacity to invade into surrounding tissue and migrate to distant sites. The tumor-specific factors that drive EMT aren't completely understood; however, evidence implicates inflammation in this process. In this issue of the Journal of Clinical Investigation, a team led by Heiko Hermeking at Ludwigs-Maximilians University determined that exposure of human colorectal cancer cells to the proinflammatory cytokine IL-6 activates the oncogenic transcription factor STAT3, which represses the gene encoding microRNA-34a (miR-34a) and promotes mesenchymal phenotypes. The IL-6 receptor (IL-6R) was identified as a direct target of miR-34a, defining an IL-6R/STAT3/miR-34a feedback loop that promotes EMT, invasion, and metastasis. Activation of p53, which induces miR-34a, decreased IL-6-dependent invasion and migration via reduced IL-6R expression, while loss of miR-34a in a murine model of colitis-associated cancer resulted in enhanced. In an accompanying Commentary, Raghu Kalluri and colleagues of the University of Texas MD Anderson Cancer Center discuss the role of tumor microenvironment in promoting EMT and metastasis.

TITLE: IL-6R/STAT3/miR-34a feedback loop promotes EMT-mediated colorectal cancer invasion and metastasis

AUTHOR CONTACT: Heiko Hermeking
Ludwigs-Maximilians University, Munich, , DEU
Phone: 011-49-89-2180-73685; Fax: 011-49-89-2180-73697; E-m
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Contact: Corinne Williams
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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