Special Issue "Activations of Cadherin Signaling in Cancer"
Deadline for manuscript submissions: closed (31 January 2021) | Viewed by 45765
The members of the cadherin superfamily are cell–cell adhesion molecules, which are an important determinant of cellular interactions and tissue morphogenesis during development and are essential for the maintenance of adult tissue architecture.
In various types of cancer, cadherins and cadherin-associated or -related proteins are now thought to contribute at different levels to suppression, or initiation, or progression. Indeed, cadherins might act as signaling scaffolds for growth factor signalings, membrane trafficking networks, cytoskeletal remodeling, cell shape and polarity, and gene expression programs, thus positively or negatively contributing to proliferation and cell motility. For metastatic dissemination, the current model involves the process of the epithelial‐to‐mesenchymal transition (EMT), in which cancer cells undergo to the so-called ‘cadherin switch’, partially or completely losing their epithelial properties, detach and move as single cells, and form clonal metastases. Following novel and intriguing investigations, another theory is emerging of collective ‘epithelial metastases’, whereby groups of cancer cells invade and disseminate collectively to establish multiclonal metastases. Other regulatory mechanisms govern cadherin gene expression, trafficking, and processing, and these events integrate with other cellular signaling pathways to drive cancer cell behavior.
This Special Issue calls for original research, full reviews, and perspectives that address, in cancer cells, the current knowledge and the progress in understanding signaling involving cadherins, as well as efforts to develop inhibitors of pro-tumorigenic interactions. Contributions are not limited to the fields mentioned in the keywords.
Dr. Antonella Tomassetti
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- Catenin, actin cytoskeleton
- Gene expression
- Protein degradation