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R.E. Mansel et al. (eds.), Metastasis of Breast Cancer, 77-110. © 2007 Springer.

Early studies demonstrated a correlation between the reduction of TJs and tumour differentiation and experimental evidence has emerged to place TJs in the frontline as the structure that cancer cells must overcome in order to metastasize (6-9) (Figure 1). Although a considerable body of work exists on TJs and their role in a number of diseases, it is only in the last few years that their possible role in tumorigenesis has been studied and to date most of the work has been concentrated on cell lines and to a limited degree on colorectal and pancreatic cancers, with a few studies carried out on breast cancer which have concentrated on Claudin-1 (SEMP-1), Claudin-7, ZO-1 and ZO-2 expression (9-16) of which, more detail later.

Changes in expression of TJ proteins may be due to regulatory mechanisms or promoter methylation. Regulatory mechanisms may be via the suggested pathway of the epithelial-mesenchymal-transition (EMT) as the process of acquisition of an invasive phenotype by tumours of epithelial origin can be regarded as a pathological version EMT (17-18). TJ determine epithelial cell polarity and disappear during EMT. Snail and Slug are factors thought to be responsible for this loss (19). Regulation also occurs via the Rho GTPase family, which is able to regulate TJ assembly (20). Thus the TJ can be regulated in response to physiological and tissue-specific requirements (4). TJs are able to rapidly change their permeability and functional properties in response to stimuli, permiting dymanic fluxes of ions and solutes in addition to the passage of whole cells (21).

This chapter will overview the recent progress in elucidating the role of TJs in the invasion and metastasis of breast cancer via changes in expression of TJ proteins and alterations in the structure of the TJ itself.

Figure 1. A schematic illustrating the structures between endothelial and epithelial cells. The TJ is located at the most apical membrane between adjacent cells.
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