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. 2021 Sep 22;40:299. doi: 10.1186/s13046-021-02090-7

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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 — miR-145-5p sponging activity inhibits PKM2 and is involved in the oncogenic roles of LNCAROD in HCC. A Dual luciferase reporter assay determined the relative luciferase activities in HCC cells following the indicated transfection. B Effect of LNCAROD overexpression on miR-145-5p level in HCC cells. C RIP assay evaluated the relative enrichment of LNCAROD and miR-145-5p in anti-IgG- or anti-AGO2-specific immunoprecipitate. D RNA pull-down assay was used to detect the interaction among LNCAROD, miR-145-5p, and AGO2. E Dual luciferase reporter assay determined the relative luciferase activities in HCC cells following the indicated transfection. F-G Alteration of PKM1/PKM2 levels after the overexpression of miR-145-5p. H-I Effect of miR-145-5p on LNCAROD mediated alteration of PKM2 levels. Data are shown as the mean ± SD. ^*P < 0.05; ^**P < 0.01