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Carcinogenesis Advance Access published online on June 13, 2006
Carcinogenesis, doi:10.1093/carcin/bgl081
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received November 10, 2005
Revised May 17, 2006
Accepted May 17, 2006

CANCER BIOLOGY

Reduced expression of CYLD in human colon and hepatocellular carcinomas

Claus Hellerbrand 1 * #, Elisabeth Bumes 2 #, Frauke Bataille 2, Wolfgang Dietmaier 2, Ramin Massoumi 3, and Anja K. Bosserhoff 2

1 Department of Internal Medicine I, University Regensburg, 93053 Regensburg, Germany
2 Institute of Pathology, University Regensburg, 93053 Regensburg, Germany
3 Department of Molecular Medicine, MPI of Biochemistry, Martinsried, Germany

* To whom correspondence should be addressed.
Claus Hellerbrand, E-mail: claus.hellerbrand{at}klinik.uni-regensburg.de


  Abstract

CYLD was originally identified as a tumor suppressor that is mutated in familial cylindromatosis. Recent studies suggested a role for CYLD in NF-{kappa}B regulation. NF-{kappa}B activation has been connected with multiple aspects of oncogenesis but the underlying molecular mechanisms of persistent NF-{kappa}B activation in tumors remain largely unknown. Thus, we evaluated CYLD transcription in different colon and hepatocellular carcinoma cell lines and tissue samples, respectively. CYLD was down regulated or lost in all tumor cell lines investigated as compared to primary human colonic epithelial cells and hepatocytes, respectively. Further, quantitative PCR analysis revealed reduced CYLD mRNA expression in most tumor samples compared to non-tumorous tissue. Analysis on protein level confirmed these findings. Functional assays with CYLD transfected cell lines revealed that CYLD expression decreased NF-{kappa}B activity. Thus, functional relevant loss of CYLD expression may contribute to tumor development and progression, and may provide a new target for therapeutic strategies.

Keywords: CYLD; tumor-suppressor gene; NF-{kappa}B signaling; hepatocellular carcinoma; colon carcinoma; cancer.
# both authors contributed equally
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