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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. 4 — Enhanced glycolysis is critically implicated in LNCAROD-induced HCC malignant behaviors. A Heatmap showing the differentially expressed genes following LNCAROD knockdown. B KEGG analysis of the enriched pathways in HCC cells with LNCAROD knockdown. Effects of LNCAROD knockdown on (C) glucose consumption (top), lactate production (middle), and ATP production (bottom) and (D) extracellular acidification rate (ECAR) in SNU-449 and HCC-LM3 cells. Effect of 2-deoxy-D-glucose (2-DG) treatment on the (E) viability, (F) colony formation, (G) migration and invasion, and (H) EMT marker expression of HCC cells. I Effect of LNCAROD knockdown on the mRNA expression of PKM1, PKM2, and PFKL in HCC cells. Data are shown as the mean ± SD. ^*P < 0.05; ^**P < 0.01