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. 2021 Mar 8;21(5):470. doi: 10.3892/etm.2021.9901

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Copyright: © Wang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Effects of S100P and RAGE on C666-1 cell migration. (A) Representative images of the wound healing assay (magnification, x400). (B) Measurements of the wound in the cell monolayer revealed that wound closure was induced by treatment with S100P protein and delayed by treatment with the RAGE inhibitor FPS-ZM1 compared with the untreated control. (C) The percentage of wound closure was different in the S100P protein and FPS-ZM1 groups compared with the untreated control group. (D) Representative images of the Transwell assay results. Scale bar, 200 µm. (E) The Transwell assay revealed that the migration ability of C666-1 cells was significantly increased by S100P protein and significantly reduced by the RAGE inhibitor FPS-ZM1. RAGE, receptor for activated glycation end products. ^***P<0.001.