Abstract
It has been known for some time that cell-cell adhesion mediated by E-cadherin and catenins is important for development and cancer in epithelial tissues. Although β-catenin is upregulated in many cancers, p120-catenin is downregulated in most human cancers. Before this study, the molecular mechanism underlying β-catenin function in tumorigenesis was well on its way to being worked out, but little was known about p120. This paper piqued my interest because it showed that p120 was a major regulator of E-cadherin stability in the salivary gland. Its loss caused a major decrease in E-cadherin with severe defects in cell-cell adhesion and tissue morphology resembling intraepithelial hyperplasia. I liked this paper because it made me think about how looking at development gives important insights into cancer and about how two related molecules that bind to E-cadherin could behave in opposite ways to get the initial phases of tumorigenesis started. This PaperPick refers to Blocked Acinar Development, E-Cadherin Reduction, and Intraepithelial Neoplasia upon Ablation of p120-Catenin in the Mouse Salivary Gland, by M.A. Davis and A.B. Reynolds, published in January 2006. Video Abstract Albert Reynolds discusses how his group came to examine the role of p120-catenin in the mouse salivary gland and the implications of their findings.
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