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Cells use different means to communicate within and between tissues and thereby coordinate their behaviours. Following the initial observations of enigmatic long filopodia unrelated to cell movement, it became clear that the roles of cellular protrusions are not restricted to sensing functions or motility and are much more diverse than previously appreciated. Advances in live-imaging and genetic tools revealed several types of non-conventional cell protrusions and their functions, ranging from tissue patterning, proliferation and differentiation control, tissue matching and cell spacing to more unexpected roles such as priming of cell adhesion as well as bidirectional coordination of tissue movements. Here, we will highlight exciting new insights into highly diverse cell behaviours elicited by protrusions and contact-dependent cell communication, essential for embryonic development across species., (Copyright © 2018. Published by Elsevier Ltd.)

Although the infiltrative behavior of malignant gliomas is one of their most critical aspects, the mechanisms underlying it have not yet been elucidated. To migrate in the brain parenchyma, malignant glioma cells need to bypass the cell-cell contact inhibitory signals. Here we propose that the blinding of cell-cell contact sensing in gliomas is caused by an unusual mechanism of cadherin switch, involving the replacement of N-cadherin with R-cadherin (Rcad) at the cell-cell junctions and the activation of ERK and p27. In our model of malignant glioma, we found that Rcad expression is necessary and sufficient to release cells from contact inhibition of proliferation, and is necessary, although not sufficient, for overriding contact inhibition of migration and for tumorigenicity. Altogether, these observations suggest that Rcad is a potential target for malignant glioma therapies.