Transition from the noninvasive to the invasive phenotype and loss of @entity19207 in XXXX @entity694 cells.

@entity1 @entity5962 @entity189 @entity1573 @entity19207 @entity3 @entity694
Loss of epithelioid organization in @entity189 cell lines has been related to @entity3 . We investigated the invasion in vitro of various @entity1 @entity694 cell lines. Most cell lines were noninvasive into @entity1573 heart fragments, and this correlated with an epithelioid morphotype. Only cell lines COLO320DM, SW620, and variants of HCT-8 and DLD-1 were invasive and nonepithelioid. We examined in these cell lines whether invasiveness was related to changes in the structure and function of the @entity5962 /catenin complex. @entity5962 functions as an invasion suppressor and as a cell-cell adhesion molecule when linked to the cytoskeleton via @entity19207 plus beta- or gamma-catenin. All noninvasive cell lines showed @entity5962 linked to these catenins. The @entity5962 -dependent cell-cell adhesion function in these cell lines was demonstrated by two assays in vitro. It was interesting that all invasive cell lines showed a dysfunctional @entity5962 /catenin complex. COLO320DM, SW480, and SW620 cells were defective in @entity5962 expression, whereas the invasive variants of HCT-8 and DLD-1 lacked the @entity19207 protein. From clonal epithelioid HCT-8 cultures with functional @entity5962 /catenin complexes, we subcloned, repeatedly, round cell variants that were again invasive and expressed no @entity19207 protein. Our data suggest that reproducible transformations toward a more invasive phenotype in HCT-8 cells are associated with down-regulation of @entity19207 . The mechanisms of this transformation and the level of @entity19207 down-regulation are currently investigated.
