ZEB1

By Jamshed Arslan Pharm.D.

Epithelial-Mesenchymal Transition (EMT) is the trans-differentiation of stationary epithelial cells into motile mesenchymal cells. During EMT, epithelial cells lose their junctions and apical-basal polarity, reorganize their cytoskeleton, undergo a change in the signaling cascade that defines cell shape and reprograms gene expression. Collectively, these changes increase the motility of individual cells and enables the development of an invasive phenotype.

Epithelial-mesenchymal transition (EMT) is a natural process by which epithelial cells lose their polarity and intercellular adhesion, and gain the migratory invasive properties of mesenchymal stem cells that can differentiate into a variety of cell types. EMT is critical to many developmental processes including embryo development and wound healing. However, EMT is also a fundamental step in the initiation of metastasis during cancer progression.

CD63 is a type II membrane protein belonging to tetraspanin superfamily and it play key roles in the activation of several cellular signaling cascades along with acting as TIMP1 receptor. It is expressed by activated platelets, monocytes, macrophages, granulocytes, T /B cells, and different type of cancer cells. CD63 localizes to endosomes, lysosomes and on the cellular surfaces, and is often considered as a marker for late endosomes as well as for lysosomes.

Beta Catenin is a cytosolic, 88 kDa intracellular protein that tightly associates with cell surface cadherin glycoproteins. It is one member of the catenin family that includes alpha Catenin, beta Catenin, and gamma Catenin. Colocalization studies using beta-catenin antibodies demonstrate that beta-catenin is a crucial link between cytoplasmic, cytoskeletal actin and transmembrane cadherin for tight cell-to-cell adhesion (1,2).