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Cell migration in 3D ECM Review article Tumor-cell invasion and migration: diversity and escape mechanisms Nature Review 2003 (3)

Cell migration in 3D ECM

Many studies confirm that the multistep model of cell migration applies to cancer cells. ECM-degrading enzymes, such as matrix metalloproteinases (MMPs) are frequently upregulated in tumor cells, and facilitate migration in vitro, as well as dissemination and metastasis in vivo. The overexpression or activation of the Rac, Rho, ROCK or MLCK signaling pathways have been correlated with in vitro tumor cell migration, as well as in vivo invasion and progression. Pharmacological inhibitors that block integrins, MMPs, ROCK or MLCK are being developed to interfere with cancer-cell invasion. Cancer therapeutics designed to target adhesion receptors or proteases have not yet been show to be effective in clinical trials. This might be due to the fact that the cancer cell’s migration mechanisms can be reprogrammed, allowing it to maintain its invasive properties via morphological and functional de- differentiation.

* Epithelial-Mesenchymal Transition (EMT)

* Intercellular junctional complex apical basal

Cell-cell adhesion results from interaction between extracellular domains of cadherins from opposing cells to form a "cell adhesion zipper", which, if extensive, would hold cells together with great strength different cell types might engage in different types of interactions   The greater the number of interacting cadherins in a cluster, the greater the strength of adhesion between apposing cells

Embryonic development is characterized by changes in gene expression, cell shape, cell motility, cell adhesion, etc. Mesenchyme (loose, primarily nonadhesive cells) Epithelium (tightly adherent, organized cell layer) * mesenchymal-epithelial transition N-cadherin

Sites of EMT and MET in the emergence and progression of carcinoma. Nature, Vol. 2,

Drivers and mediators of EMT. Cell, Vol. 118, The morphological transition of EMT was accompanied by scattering and directional migration toward serum factors, a gain of mesenchymal cell markers (fibronectin, vimentin, and N-cadherin), and a loss of epithelial markers (E-cadherin, and  - and g-catenin).