alexa Securin (hPTTG1) expression is regulated by beta-catenin TCF in human colorectal carcinoma.
Genetics & Molecular Biology

Genetics & Molecular Biology

Journal of Down Syndrome & Chromosome Abnormalities

Author(s): Hlubek F, Pfeiffer S, Budczies J, Spaderna S, Jung A

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Abstract

Overexpression of the transcriptional activator beta-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 beta-catenin and securin (hPTTG1) in colorectal adenomas and carcinomas and further demonstrate that securin is a target of beta-catenin transcriptional activation. This implies that deregulation of the beta-catenin/T-cell factor-signalling pathway leads to overexpression of securin in human colorectal cancer, which subsequently may contribute to tumour progression.

This article was published in Br J Cancer and referenced in Journal of Down Syndrome & Chromosome Abnormalities

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