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Abstract

The invasion-suppressor molecule E-cadherin mediates Cal2+-dependent cell aggregation and prevents invasion. E-cadherin-positive Madin-Darby canine kidney (MDCK) cells that were non-invasive in vitro formed, upon i.p. injection, tumors that were invasive. Differentiated tubular tumor areas showed an intense immuno-signal for E-cadherin at intercellular contacts, whereas undefferentiated structures did not. Cell lines derived from such tumors turned out to be invasive in vitro and showed decreased Ca2+-dependent cell aggregation but no change in E-cadherin immunopositivitv. This combination of phenotypes indicated a loss of the E-cadherin invasion-suppressor function-Mi cro-en capsulation of i.p.-injected cells prevented the loss of the E-cadherin invasion-suppressor function. We concluded that this loss in vivo was dependent upon immediate contacts between tumor cells and host cells or upon host factors that could not cross the capsule membrane. © Wiley-Liss, Inc.