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. 2021 May 26;40:177. doi: 10.1186/s13046-021-01973-z

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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. 8 — DLX6-AS1 mediates miR-15a-5p to target CXCL17 to drive migration, invasion and EMT in HCC. a. RT-qPCR analysis of CXCL17 expression in clinical tissues; b. RT-qPCR and Western blot analysis of CXCL17 expression in cancer cells and normal liver cells; c. RT-qPCR and Western blot analysis of CXCL17 expression in macrophages after down-regulating miR-15a-5p; d. Prediction of the potential binding site of miR-15a-5p and CXCL17 through bioinformatics websites; e. Verification of the targeting relationship between miR-15a-5p and CXCL17 through dual luciferase reporter experiment; data were expressed as mean ± standard deviation (repetition = 3) and evaluated by One-way AVONA and Tukey’s test. $ P < 0.05 compared with HL-7702 cells; & P < 0.05 compared with the NC-inhibitor group