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JCI online early table of contents: Sept. 13, 2010
Date:9/13/2010

42;
E-mail: jean-pierre.hardelin@pasteur.fr.

View this article at: http://www.jci.org/articles/view/43699?key=c10e3ab8d55ad855aca1


ONCOLOGY What's SMAD-da u?

The TGF-beta signaling pathway can be tumor suppressing or promoting depending on the tumor stage and context. One of the potential TGF-beta target genes involved in its dual effects of on cancer is hepatocyte growth factor (HGF), which, acting through c-Met, can lead to the proliferation, survival, invasion, and migration of tumor cells and angiogenesis in tumor stroma. In human squamous cell carcinomas (SCCs), the TGF-beta signaling pathway components Smad2 and Smad4 are often down regulated. In this issue of the JCI, Xiao-Jing Wang and colleagues, of the University of Colorado, Denver, investigated the role of this signaling pathway in skin cancer by chemically inducing cancer in mice that lacked Smad2 specifically in the skin. SCCs in these mice showed increased blood vessel density and increased levels of HGF. Further analysis revealed a repressive role for Smad2 in expression from the HGF gene, countered by an activating role for Smad4 on the same gene. The authors believe that their findings suggest that analysis of Smad expression in human tumors may be an important biomarker that will allow for the development of better targeted therapies in the future.

TITLE:

HGF upregulation contributes to angiogenesis in mice with keratinocyte-specific Smad2 deletion

AUTHOR CONTACT:
Xiao-Jing Wang,
University of Colorado, Denver, Aurora, Colorado, USA.
Phone: 303.724.3001; Fax: 303.724.3712; E-mail: xj.wang@ucdenver.edu.

View this article at: http://www.jci.org/articles/
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Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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