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. 2016 May 30;7(28):43907–43923. doi: 10.18632/oncotarget.9724

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Copyright: © 2016 Pajari et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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A. HGF activates AKT and ERK in HT29 and HCA7 colon adenocarcinoma cells as shown by western blot analysis. B. Scratch wound healing is dependent on PI3K/AKT and ERK activation as treating the HT29 cells with the PI3K inhibitor LY294002 (LY) and the MAPKK (MEK) inhibitor U0126 prevents wound closure as determined by time-lapse microscopy. C. Wound areas in HGF-stimulated HT29 cells treated with LY294002 (mean from two independent experiments), U0126 (one experiment) and without inhibitors (mean from 3 independent experiments) were analyzed quantitatively every 5 min by determining the percentage of remaining wound area as compared to the area of the wound at time 0.