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. 2016 Sep 12;5(9):e258. doi: 10.1038/oncsis.2016.59

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Copyright © 2016 The Author(s)

Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 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/4.0/

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ARHGEF5 KD suppresses the invasive activity of human colorectal cancer HCT116 cells. (a) ARHGEF5 in HCT116 cells was knocked down with siRNAs (siGEF5 no. 1 and siGEF5 no. 3) in HCT116 cells and downregulation of ARHGEF5 confirmed by western blotting (upper). Control and siRNA-treated HCT116 were stained for F-actin. Scale bar: 20 μm. (b) Control and siRNA-treated HCT116 cells were subjected to an in vitro wound-healing assay. Scale bar: 200 μm. Values represent the mean±s.d. (n=3, **P<0.01). (c) The in vitro invasive activity of control HCT116 cells and those treated with specific siRNAs was examined in a Matrigel Transwell assay. Yellow arrowheads indicate invaded cells. Scale bar: 20 μm. Values represent the mean±s.d. (n = 3, *P<0.05). (d) The in vivo metastatic activity of HCT116 cells transfected with control and shGEF no. 1 was examined in experimental metastasis assays in nude mice. Metastatic lesions were observed by staining tissue slices with hematoxylin–eosin. Black arrowheads indicate metastatic lesions. Magnified views of the lesions in mice C4 and C5 are shown.