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Open Access 01-12-2022 | osteosarcoma | Correction
Correction to: CCR9 initiates epithelial–mesenchymal transition by activating Wnt/β-catenin pathways to promote osteosarcoma metastasis
Published in: Cancer Cell International | Issue 1/2022
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In this article [1], the annotation was wrong in Fig. 5B and in Fig. 6C, the figure of HOS cells treated by OE-CCR9 + XAV 939 at 0 h was wrong. The revised Figure 5 and its legend and Figure 6 are given below.
Fig. 5
a The GSEA results showed significant enrichment of the gene signature associated with EMT and cell adhesion molecules. b The protein expression level of E-cadherin was lower in OS tissues with lung metastasis, and the expression of N-cadherin and Vimentin was upregulated. c The expression N-cadherin, vimentin, twist, snail and MMP-1, was obviously downregulated, and E-cadherin expression was significantly upregulated in si-CCR9 group. d The protein expression levels of EMT-related markers in MG63 and HOS cells. e Quantitative data for the protein expression levels of EMT-related markers. Mean ± SD from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001
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
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