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. 2020 May 22;5:54. doi: 10.1038/s41392-020-0152-8

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© The Author(s) 2020

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 — GBE1 induces metabolic reprogramming in LUAD cells. a Seahorse metabolic analysis of ECARs and OCRs in the shGBE1 and shNC A549 cells. b Intracellular 2-NBDG accumulation evaluation in the shGBE1 and shNC A549 cells. c, d The effect of GBE1 knockdown in the A549 cells on lactate production (c) and ATP secretion (d). e The correlation between GBE1 expression levels in the LUAD tissues with Glut1 and LDHA expression levels in the samples in the TCGA data set. f ROS expression in the shGBE1 and shNC A549 cells was analyzed by fluorescence imaging and flow cytometry. g The ratio of NADP/NADPH in the shGBE1 and shNC A549 cells. h RNA-seq and i pan-metabolomic analysis of GBE1 knockdown in the A549 cells. j Heat map showing the fold changes of differentially expressed genes based on the glucose metabolism PCR array. k Schematic illustration of changes in metabolic signaling pathways induced by GBE1 knockdown. Data are represented as the means ± SD. **P < 0.01, ***P < 0.001