Cell polarity signaling in the plasticity of cancer cell invasiveness

Aneta Gandalovičová _, Tomáš Vomastek, Daniel Rosel and Jan Brábek

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Oncotarget. 2016; 7:25022-25049. https://doi.org/10.18632/oncotarget.7214

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Aneta Gandalovičová1, Tomáš Vomastek2, Daniel Rosel1 and Jan Brábek 1

1 Department of Cell Biology, Charles University in Prague, Viničná, Prague, Czech Republic

2 Institute of Microbiology, Academy of Sciences of The Czech Republic, Videňská, Prague, Czech Republic

Correspondence to:

Jan Brábek, email:

Keywords: polarity, invasion, plasticity, EMT, AMT

Received: May 25, 2015 Accepted: January 29, 2016 Published: February 08, 2016


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.

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