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. 2021 Feb 8;12(2):162. doi: 10.1038/s41419-021-03450-z

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© The Author(s) 2021, corrected publication 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A Enrichment analysis of ECT2 pathway functions in the TCGA-LIHC cohort. B, C Western blot analysis of p-AKT, PLK1, and AKT expression levels after ECT2 knockdown or PLK1 upregulation in the HepG2 cell line. D Western blot analysis of p-AKT, PLK1, and AKT expression levels after ECT2 knockdown in the PTEN-missing cell line of HCC. E Glucose intake by cancer cells was evaluated after ECT2 knockdown. F Lactate acid production by cancer cells was evaluated after ECT2 knockdown. Error bars represent means ± SD. *p < 0.05, **p < 0.01. NS means “not significant” by paired two-sided Student’s t-test.