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. 2016 Feb 4;7(2):e2088. doi: 10.1038/cddis.2015.274

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Copyright © 2016 Macmillan Publishers Limited

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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Knockdown of c-Met suppresses BCa cells motility. (a) UM-UC-3 cells were transfected with NC, miR-433 mimics, siMet, and siCREB1, respectively. Wound-healing assay was performed with a 24-h recovery period. (b) Transwell assay (representative micrographs were presented). siMet impaired the motility of T24 and UM-UC-3 cells. (c) siMet inhibited EMT and AKT/GSK-3β signaling-related proteins in T24 and UM-UC-3 cells. (d) Representative images of IHC staining of TMA. c-Met showed a membranous and cytoplasmic location. (e) Statistical analysis indicated that the expression level of c-Met protein in BCa tissues was significantly higher than that in adjacent non-tumor tissues. (f) Kaplan–Meier survival analysis. The protein expression of c-Met was not associated with the overall survival rate in BCa patients. Error bars represent the S.E. obtained from three independent experiments; *P<0.05. Scale bars=100 μm.