The role of desmosomal cadherins in colorectal tumourigenesis

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http://eprints.org/relation/isVersionOf http://etheses.bham.ac.uk/id/document/28740 http://eprints.org/relation/isVolatileVersionOf http://etheses.bham.ac.uk/id/document/28740 http://eprints.org/relation/isIndexCodesVersionOf http://etheses.bham.ac.uk/id/document/28740 archive 4031 disk0/00/00/34/66 2013-04-26 17:11:44 2019-01-23 09:56:20 2013-04-26 17:11:44 thesis show 0 McEvoy Katherina Yasmin Chidgey Martyn Morton Dion University of Birmingham The role of desmosomal cadherins in colorectal tumourigenesis unpub RC0254 10col_mede In cancer, loss of intercellular contact contributes to tumour progression and invasion. Desmosomal cadherins are essential constituents of desmosomes – intercellular junctions that confer significant adhesive strength to epithelial tissues and cardiac muscle. Although changes in desmosomal components have been noted in a variety of cancers previously, this investigation has shown for the first time altered desmocollin expression in colorectal cancer. Real-time PCR and western blotting were used to assess desmocollin expression in a series of colorectal cancer and matched normal tissue samples. Loss of desmocollin 2 expression was observed in the cancer samples. In addition, de novo expression of desmocollins 1 and 3, which are not normally expressed in the colon, was observed. Desmoglein gene expression was also altered in the cancer samples. Although classical cadherin switching is a hallmark of the epithelial-mesenchymal transition, desmocollin switching has not previously been reported. Further experiments, to investigate the effect of loss of desmocollin 2 and desmoglein 2 on the behaviour of cultured cells were performed. In addition, experiments were carried out to identify those transcription factors that regulate desmosomal cadherin gene expression in the colon. Transcription factors of the CCAAT/enhancer-binding proteins family act as transcriptional activators of desmosomal cadherin promoters in colonic cells. 2012-12 2012-05 graduation eng author This unpublished thesis/dissertation is copyright of the author and/or third parties. The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation. Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged. Further distribution or reproduction in any format is prohibited without the permission of the copyright holder. public 199 University of Birmingham Institute of Cancer Studies h_md na 2012-12 graduation