Abstract
Apico-basal polarity is typical of cells present in differentiated epithelium while front-rear polarity develops in motile cells. In cancer development, the transition from epithelial to migratory polarity may be seen as the hallmark of cancer progression to an invasive and metastatic disease. Despite the morphological and functional dissimilarity, both epithelial and migratory polarity are controlled by a common set of polarity complexes Par, Scribble and Crumbs, phosphoinositides, and small Rho GTPases Rac, Rho and Cdc42. In epithelial tissues, their mutual interplay ensures apico-basal and planar cell polarity. Accordingly, altered functions of these polarity determinants lead to disrupted cell-cell adhesions, cytoskeleton rearrangements and overall loss of epithelial homeostasis. Polarity proteins are further engaged in diverse interactions that promote the establishment of front-rear polarity, and they help cancer cells to adopt different invasion modes. Invading cancer cells can employ either the collective, mesenchymal or amoeboid invasion modes or actively switch between them and gain intermediate phenotypes. Elucidation of the role of polarity proteins during these invasion modes and the associated transitions is a necessary step towards understanding the complex problem of metastasis. In this review we summarize the current knowledge of the role of cell polarity signaling in the plasticity of cancer cell invasiveness.
Highlights
Cell movement is an important process in every multi-cellular organism, central to morphogenesis especially in organisms lacking cell walls
In this review we focus on the mechanisms and processes underlying the plasticity of cell invasion that were documented in metazoans, as a rule vertebrates, unless stated otherwise
Loss of epithelial polarity and de-differentiation of epithelial cells are crucial for establishment of the migratory and invasive polarity, which underlies efficient metastatic spread of cancer cells
Summary
Cell movement is an important process in every multi-cellular organism, central to morphogenesis especially in organisms lacking cell walls. Cancer associated EMT represses the function of polarity and cell-cell adhesion complexes and, on the other hand, induces expression of mesenchymal and pro-migratory genes (reviewed in [9, 10]). Cells migrating individually in a mesenchymal manner can undergo a process opposite to EMT, during which they lose motility, settle, retain cellular junctions and differentiate to form multicellular epithelial structures (Figure 1).
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