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. 2019 Sep 27;9:992. doi: 10.3389/fonc.2019.00992

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Copyright © 2019 Kalli, Voutouri, Minia, Pliaka, Fotis, Alexopoulos and Stylianopoulos.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed mechanism of this study. The proposed mechanism of the present study is that compressive force, applied on brain cancer cells, could activate MEK1/Erk1 pathway through EGFR/Ras/Raf activation, which as it is widely known, is just upstream of MEK1. Subsequently, MEK1/Erk1 could regulate the expression of several migration-related genes including GDF15, in order to re-organize the compression-disrupted actin cytoskeleton, which eventually facilitates cell migration. Finally, through a possible negative feedback loop, GDF15 could bind to its receptor and then suppress MEK1/Erk1 activation in order to regulate its levels in compressed cells. In this diagram, the arrows are of different width, so that thick arrows indicate a stronger compression-induced effect in the less aggressive cells, while thin arrows indicate a weaker effect in the highly aggressive cells, which could permit a possible tumor suppressing pathway to hinder the compression-induced MEK1/Erk1 mediated migratory effect.