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. 2017 Jul 31;36(47):6542–6554. doi: 10.1038/onc.2017.262

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Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

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Schematic model of how ROS1 promotes oral cancer progression. Higher level of miR-200a-3p correlates with low EZH2 and enhanced OSCC invasion. The reduction of EZH2 level in the highly invasive OSCC cells relieves H3K27m3 modification and opens chromatin for transcriptional activation of ROS1 as well as a number of novel ROS1 target genes. Elevated ROS1 activates the MEK-ERK1/2 and PI3K-AKT pathways to increase STAT1 occupancy at the regulatory regions of GLI1 and CXCL1 to promote cell proliferation and invasion.