ules, chemokines, cell-cell adhesion molecules, and extracellular proteases (Bogenrieder & Herlyn, 2003). This review will analyze the mechanisms of function and expression of cadherin (an intercellular adhesion protein) in the first stage of metastasis where cell adhesion is decreased at the primary tumor.
In studying cancer, model organisms provide insight into the molecular basis and alterations occurring in the disease as well as detection and treatment methods. Creating cancer models through genetic alterations has been mastered in the mouse. Gene modifications, when used together with powerful cytogenic techniques, provide the best methodology for cancer research (Resor, Bowen, & Wynshaw-Boris, 2001). On the other hand, cancer studies of cultured cell lines from biopsied human carcinomas are becoming increasingly popular. A human tumor model is most genetically comparable to in vivo cancer, and cellular analysis as well as detection of the metastatic process is highly useful as it can be directly applied in medicine.
Cadherins are cell-cell adhesion molecules involved in tissue architecture, and are members of the cell adhesion molecule (CAM) family. Their structure is defined by two glycoprotein single transmembrane domains forming a dimer. Cells adhere via Ca2+-dependent assembly of opposite extracellular cadherin dimers in a zipper-like manner (Fig. 2).
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