Severe polyposis in Apc(1322T) mice is associated with submaximal Wnt signalling and increased expression of the stem cell marker Lgr5

Annabelle Lewis, Stefania Segditsas, Maesha Deheragoda, Patrick Pollard, Rosemary Jeffery, Emma Nye, Helen Lockstone, Hayley Davis, Susan Clark, Gordon Stamp, Richard Poulsom, Nicholas Wright, Ian Tomlinson

Research output: Contribution to journalArticlepeer-review

Abstract

Adenomatous polyposis coli (APC) is a tumour suppressor gene mutated in the germline of patients with familial adenomatous polyposis (FAP) and somatically in most colorectal cancers. APC mutations impair β-catenin degradation, resulting in increased Wnt signalling. The most frequent APC mutation is a codon 1309 truncation that is associated with severe FAP. A previous study compared two mouse models of intestinal tumorigenesis, Apc(R850X) (Min) and Apc(1322T) (1322T), the latter a model of human codon 1309 changes. 1322T mice had more severe polyposis but, surprisingly, these tumours had lower levels of nuclear β-catenin than Min tumours. The consequences of these different β-catenin levels were investigated.
Original languageEnglish
Pages (from-to)1680-6
Number of pages7
JournalGut
Volume59
Issue number12
DOIs
Publication statusPublished - Dec 2010

Keywords

  • Adenomatous Polyposis Coli
  • Animals
  • Gene Expression Profiling
  • Gene Expression Regulation, Neoplastic
  • Genes, APC
  • Mice
  • Mice, Inbred C57BL
  • Microdissection
  • Neoplasm Proteins
  • Receptors, G-Protein-Coupled
  • Signal Transduction
  • Wnt Proteins

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