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Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
Involvement of μ-protocadherin in colorectal carcinogenesis: a promise for clinico-pathological evaluation
1Department of Life Sciences, University of Modena and Reggio Emilia, Modena, Italy. lorena.losi@unimore.it.
Abstract:
Cell-cell adhesion is a fundamental activity to allow the maintenance of epithelial integrity, and defects impairing this process promote the formation of tumors such as colorectal cancer (CRC). In this regard, a crucial role is played by adhesion molecules, named cadherins, which exert their function through the inhibition of the β-catenin signaling proliferation pathway, constitutively activated in CRC. A number of reports, published over the last decade, have highlighted the existence of a novel cadherin family member, called μ-protocadherin, to underline the hybrid nature of its extra-cellular region, including both cadherin-like and mucin-like domains. Is has been shown that this protein plays an important role in inter-cellular adhesion processes, inhibits β-catenin activity in normal colorectal mucosa, undergoes a down-regulated expression in CRC and is up-regulated upon treatment with chemoprevention agents against this tumor.
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