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. 2020 Sep 29;20:468. doi: 10.1186/s12935-020-01568-2

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© The Author(s) 2020

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. 3 — SOX4 binds to the promoter of the CXCR7 gene and activates its transcription. a Increased amount of CXCR7 mRNA in SOX4-expressing MDA-MB-231 and SUM149 cells. The data are presented as the mean ± s.d. of triple wells. Unpaired two-tailed t-test: *p < 0.05, **p < 0.01. b CXCR7 gene fragments amplified from pull-down samples of the chromatin immunoprecipitation assay using the SOX4 antibody and non-specific IgG, and the input samples. c Dual-luciferase reporter assay showing increased CXCR7 promoter-specific reporter activity associated with SOX4 overexpression. d and e CXCR7 inhibitor CCX771 (ccx) reversed the enhancing effect of SOX4 on migration and invasion. The data are presented as the mean ± s.d. of triplicate wells. Unpaired two-tailed t-test: *p < 0.05, ***p < 0.001. f IHC analysis of SOX4 and CXCR7 expression in human breast primary tumors (Primary) and lymph node metastatic foci (LN)