1. ¹Department of Pathology, Ludwig-Maximilians University of Munich, Thalkirchner Str. 36, 80337 Munich, Germany
2. ²oligene GmbH, Campus Charité Mitte, Schumannstr. 20/21, 10117 Berlin, Germany
3. ³Department of Pathology, University of Erlangen-Nürnberg, Krankenhausstr. 8-10, 91054, Erlangen, Germany

Correspondence: Dr F Hlubek, E-mail: Falk.Hlubek@med.uni-muenchen.de

Revised 15 March 2006; Accepted 5 April 2006; Published online 16 May 2006.

Abstract

Overexpression of the transcriptional activator -catenin, mostly owing to loss-of-function mutations of the adenomatous polyposis coli (APC) tumour suppressor gene, is crucial for the initiation and progression of human colorectal carcinogenesis. Securin is a regulator of chromosome separation and its overexpression has been shown to be involved in different tumour-promoting processes, like transformation, hyperproliferation and angiogenesis, and correlates with tumour cell invasion. However, the molecular mechanism leading to securin overexpression in human colorectal cancer is unknown. Here we show a correlated high expression of -catenin and securin (hPTTG1) in colorectal adenomas and carcinomas and further demonstrate that securin is a target of -catenin transcriptional activation. This implies that deregulation of the -catenin/T-cell factor-signalling pathway leads to overexpression of securin in human colorectal cancer, which subsequently may contribute to tumour progression.