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. 2016 Nov 24;7(11):e2480. doi: 10.1038/cddis.2016.225

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Copyright © 2016 The Author(s)

Cell Death and Disease 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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FOXK1 enhances c-jun-mediated participation in GC cell growth, migration and invasion. (a) C-jun expression levels were detected using western blot analysis in MKN28 cells, which were transfected with FOXK1 overexpression plasmids. This was followed by transfection with c-jun small interfering RNA (siRNA) or Scr siRNA as a negative control. (b) Stable transfectants of FOXK1 were then transfected with c-jun siRNA or Scr siRNA, cultured in complete medium for 24, 48 and 72 h and evaluated using a WST-8 assay. ****P<0.0001, between FOXK1-c-jun siRNA and FOXK1-Src siRNA. (c) MKN28-stable transfectants of FOXK1 after transfection with c-jun siRNA or Scr siRNA for 48 h were subjected to an EdU (5-ethynyl-2′-deoxyuridine) incorporation assay. ****P<0.0001. (d) For the wound-healing experiments, cells were analyzed using live-cell microscopy. Original magnification, × 10. ***P<0.001 and ****P<0.0001. (e) MKN28-stable FOXK1 transfectants were transfected with c-jun siRNA 48 h later, and the invasive ability of the cells was decreased. ****P<0.0001. Scale bars represent 100 μm in (c)