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. 2018 May 9;8:7367. doi: 10.1038/s41598-018-25668-2

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Model of RBM3’s influences on cell morphology and migration. (a) Schematic of the morphological trajectories taken by B104 cells under control, RBM3 knockdown, and RBM3 knockdown plus ROCK inhibitor conditions. Replated B104 cells initially exhibit SICs and a rounded morphology. Whereas control cells go on to adopt a bi- or multi-polar shape, cells lacking RBM3 lose polarity and undergo exaggerated spreading. Inhibition of ROCK during replating of RBM3 knockdown cells rescues polarity but enhances process elongation. (b) Diagram of proposed mechanisms by which RBM3 regulates cell polarity and spreading. Knockdown of RBM3 results in parallel changes in translation and a RhoA-ROCK-CRMP2 pathway. Elevated RhoA expression activates ROCK, a kinase involved in the transition from a mesenchymal to an amoeboid state. Reduced levels of CRMP2, a microtubule binding protein that is inhibited by ROCK phosphorylation, contributes to loss of polarity. (c) Schematic of hypothesized effects of RBM3 expression level on transitions between mesenchymal and amoeboid states. High levels of RBM3 lock cells into a highly polar, mesenchymal like mode of migration. Low RBM3 may favor an amoeboid state, but still be permissive to transitions between amoeboid and mesenchymal modes of migration, so-called MAT and AMT, respectively. This is may enhance metastasis of cancers by enhancing migration mode flexibility.