The many genotypically different carcinomas have one commonality: the metastatic process. The stromal microenvironment surrounding neoplastic cells influences their metastasis-related functions (e.g. adhesion, survival, proteolysis, migration, immune escape, and organ targeting). Metastasis starts at the primary tumor when cells loose their adhesiveness, allowing for them to detach from the tumor and migrate. Cell-cell adhesion regulated by E-cadherin is weakened or abolished in metastatic cells. This leads to the malignant invasion of cancer. Preserving E-cadherin expression is the first step in hindering subsequent metastatic events. Within the last two years, research aimed at determining E-cadherin regulation mechanisms has been strictly performed in mouse and human cancer models. It is clear that these are the preferred models since they allow genetic manipulation and provide ways to detect and study the disease in humans. Invasive cancer is of highest concern in medicine, as it is responsible for 90% of patient deaths.
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             The most devastating of cancer properties are invasiveness and metastatic ability. Recent molecular and cellular studies have elucidated the processes underlying the metastatic cascade (Fig. 1). The steps of metastasis are: cell-cell deadhesion, invasion of the basement membrane, intravasation, entry and travel through the circulation, extravasation, and migration and growth into new secondary tissue. In vivo experiments in the mouse model have proven that tumors with impaired intracellular adhesion promote malignant invasion (Cavallaro & Christofori, 2001).
             Cell migration is a key process in cancer spreading since it facilitates metastasis. Containing tumor cells to the primary cancer site, and inhibiting cell movement at any of the metastatic steps is necessary to prevent malignant propagation. Main factors mediating cell motility are: growth factor signalling molec...