Albert B. Reynolds, PhD, University of Virginia

The Reynold's laboratory combines molecular and biochemical approaches with 3D culture and mouse models of colon and breast cancer to study the roles of p120-catenin (p120) in cell-cell adhesion, tumorigenesis and metastasis. Most proteins linked physically or functionally to p120 are, in fact, tumor suppressors or oncogenes (eg, Src, Receptor Tyrosine kinases, Rho GTPases, E-cadherin, B-catenin, Adenomatous Polyposis Coli), implying a role for p120 in cancer. Previously, they showed that p120 interaction is essential for cadherin stability at the cell surface. For example, p120 knockdown in many epithelial cell lines (eg, MCF10A, A431) causes rapid degradation of the entire E-cadherin complex and partial or complete loss of cell-cell adhesion. These observations have led to the notion that p120 itself is a tumor and/or metastasis suppressor - on its own, or in collaboration with E-cadherin. Indeed, E-cadherin is broadly established as a tumor and metastasis suppressor and p120 is frequently downregulated and/or mislocalized in most major human cancers (e.g. colon, breast, lung, pancreas, prostate).

*Now affiliated with Vanderbilt-Ingram Cancer Center

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