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. 2021 Feb 17;40:72. doi: 10.1186/s13046-021-01868-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. 7 — PLAGL2 is the direct functional target of miR-154-5p. a 10 potential targets of miR-154-5p was predicted by applying three online bioinformatics tools. b mRNA levels of three potential targets in Hep3B cell with miR-154-5p overexpression. c The effect of miR-154-5p on PLAGL2 protein level evaluated by western blotting. d The predicted binding sites between miR-154-5p and PLAGL2 and mutant sequences of the potential miR-154-5p binding site in PLAGL2. In addition, the result of luciferase reporter assay is exhibited. e Western blotting confirmed that MAPKAPK5-AS1 and miR-154-5p could reverse the regulatory effect on PLAGL2 expression reciprocally. f The expression level of PLAGL2 in HCC tissues and adjacent non-tumor tissues. g Expression association between PLAGL2 and miR-154-5p in HCC tissues. h Expression association between PLAGL2 and MAPKAPK5-AS1 in HCC tissues. *p < 0.05