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. 2022 Oct 10;11(1):61. doi: 10.1038/s41389-022-00436-0

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© The Author(s) 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. 5 — A Extracellular flux assays showing that ERRα mediated aerobic glycolysis partly depends on regulating HK2 in DV90 cell line. B EdU assays showing that ERRα mediated malignant progression partly depends on regulating HK2 in DV90 cell line. Glucose uptake, lactate excretion (C), clone formation assay (D) and EdU assay (E) showing that ERRα mediated malignant progression partly depends on regulating SEs in DV90 cell line. Clone formation assay (F) and CCK-8 assay (G) revealing the inhibitory efficacy of 2-DG, osimertinib and their combination in the EGFR^mut cluster 3-like cell line (H1975) and EGFR^mut non-cluster 3-like cell line (PC-9). H Combination index of 2-DG and osimertinib in the indicated cell lines. Combination index > 1 indicated antagonism, combination index < 1 indicated synergy.