Keratoepithelin suppresses the progression of experimental human neuroblastomas.

Abstract

Neuroblastoma is the most common extracranial childhood tumor. High expression of activin A is associated with a favorable prognosis, but the contributing mechanisms have remained unclear. Our previous demonstration of the activin A-mediated up-regulation of keratoepithelin led to the consideration that keratoepithelin could modulate neuroblastoma growth and/or progression. We report here that enhanced keratoepithelin expression in human neuroblastoma cells suppresses neuroblastoma cell cohesion and adhesion to various extracellular matrix proteins and that it inhibits neuroblastoma cell proliferation and invasion in vitro and in vivo. Using microarray analysis, we identified several keratoepithelin-regulated genes that may contribute to these biological changes. Together with the observation that keratoepithelin is expressed in human neuroblastomas in vivo, our data suggest that keratoepithelin could play a beneficial role in neuroblastoma development and/or progression.

• Authors: Jürgen Becker, Bernhard Erdlenbruch, Ievgeniia Noskova, Alexander Schramm, Monique Aumailley, Daniel F Schorderet, Lothar Schweigerer
• Journal: Cancer research (Cancer Res) Vol. 66 Issue 10 Pg. 5314-21 (May 15 2006) ISSN: 0008-5472 [Print] United States
• PMID: 16707457 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Extracellular Matrix Proteins
• Transforming Growth Factor beta
• betaIG-H3 protein

Topics

• Animals
• Cell Adhesion (physiology)
• Cell Growth Processes (physiology)
• Chick Embryo
• Disease Progression
• Extracellular Matrix Proteins (biosynthesis, genetics)
• Humans
• Mice
• Neoplasm Invasiveness
• Neuroblastoma (genetics, metabolism, pathology)
• Transfection
• Transforming Growth Factor beta (biosynthesis, genetics)