Almost without exception, what kills cancer patients is metastasis, or cancer spread, not the primary tumor. Although the process of metastasis is not well understood, it is strongly associated with the loss of a protein called E-cadherin. E-cadherin normally acts to hold cells together and is indispensable for the proper organization of tissues and organs in our bodies. When cancer cells loose the function of this protein during tumor progression, they disorganize, change shape and become more migratory and invasive. Our laboratory is investigating the mechanisms that cause loss of E-cadherin function in cancer cells and how E-cadherin accessory proteins promote cancer spread (see cancer focus). We are particularly interested in the role of one such protein, called p120 catenin (p120). When bound to E-cadherin, p120 strengthens the bonds between cells. When not associated with E-cadherin, it induces cell movement and invasiveness. Our goal is to extend our initial findings to effective treatments that prevent cancer from spreading to increase patients' long-term survival.
Interestingly, p120 is the prototypic member of a family of proteins that interact with cadherins and play important roles in cell adhesion, cytoskeletal remodeling, cell migration, neurite morphogenesis, synapse formation and neuronal plasticity (see neuroscience focus). With an extensive array of techniques and reagents, our lab is uniquely situated to make significant advances to our understanding of these critical biological processes.
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