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. 2017 Jul 24;7:6235. doi: 10.1038/s41598-017-06673-3

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© The Author(s) 2017

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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The molecular mechanism of CXB effect on OSCC proliferation, EMT programs and cancer cell motility. The expression level of selected markers of (A) nuclear transcriptional factors (TF) and cytoplasmic mediators (CM); (B) focal adhesion related proteins (FARP) and cell adhesion molecules (CAMs); (C) intermediate filament protein, membrane binding protein and surface receptors (SR) were determined between CXB-untreated and treated HSC-3 and HSC-3-RFP cells in an immunoblotting assay (also refer Supplementary Fig. 3); and (D) the inhibitory effect of CXB on EGFR (green fluorescence) was further validated by the ICC-IF assay.