Abstract
The Epithelial-Mesenchymal Transition (EMT) is an important concept in understanding the processes of oncogenesis, especially with respect to the relationship between cell proliferation and metastatic properties such as spontaneous cell motility, chemotaxic migration and tissue invasion. EMT is now recognized as a more complex phenomenon than an all-or-nothing event, in which different components of the EMT may have distinct roles in the physio-pathological regulation of cell function and which may in turn depend on differential interactions with cell constituents and metabolic products. This mini-review summarizes recent work on the induction of cancer properties in parallel with the presence of EMT activities in the presence of serine proteases, with the focus on those tumor suppressors known as “dependence” receptors such as neogenin and Deleted in Colorectal Cancer (DCC). It is concluded that various forms of partial EMT should be given more detailed investigation and consideration as the results could have valuable implications for the development of disease-specific and patient-specific therapies.
Highlights
The concept of Epithelial-Mesenchymal Transition (EMT) was founded on changes in adhesion molecules associated with proliferation, cell dis-association, de-differentiation to a more mesenchymal stem cell character and the establishment of a motile, potentially invasive phenotype [1]
We have shown that DEPENDENCE AND GUIDANCE RECEPTORS (DGRs) function may be regulated by chymotryptic serine proteases which deplete cells of their DGRs, causing increased cell migration [27], actions that may contribute to dietary effects on cancer incidence [28, 29]
This pattern of protein changes associated with a loss of DGRs is clearly different from classical descriptions of EMT, suggesting that DGR loss should be added to the list of phenomena able to induce a “partial” EMT
Summary
EMT is recognized as a more complex phenomenon than an all-or-nothing event, in which different components of the EMT may have distinct roles in the physio-pathological regulation of cell function and which may in turn depend on differential interactions with cell constituents and metabolic products. This mini-review summarizes recent work on the induction of cancer properties in parallel with the presence of EMT activities in the presence of serine proteases, with the focus on those tumor suppressors known as “dependence” receptors such as neogenin and Deleted in Colorectal Cancer (DCC).
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