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. 2021 Dec 4;21:648. doi: 10.1186/s12935-021-02320-0

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — a The protein expression levels of active β-catenin and total β-catenin were downregulated in si-CCR9 group. b The protein expression levels and quantitative data of active β-catenin and total β-catenin in MG63 and HOS cells were shown. Overexpression of CCR9 activated the Wnt/β-catenin pathway, and the Wnt signaling inhibitor XAV-939 counteracted the activation. c Cell migration assay of MG63 and HOS cells. Overexpression of CCR9 increased the wound healing rate and the inhibitor of XAV-939 inhibited this effect. d Quantification of the area percentage of wound healing. e Transwell invasion assay of MG63 and HOS cells. Overexpression of CCR9 promoted the invasion ability and the inhibitor of XAV-939 inhibited this effect. f Quantitative results of the Transwell migration and invasion assays. Mean ± SD from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001