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. 2022 Feb 4;13(2):118. doi: 10.1038/s41419-022-04576-4

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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. 6 — A PGK1 and CXCR4 were the hub genes in KIRC, and there was a strong correlation between PGK1 and CXCR4. B Co-expression of PGK1 and CXCR4 transcript levels from GSE6344 and GSE15641 dataset. C Kaplan–Meier’s survival analysis of the correlation between the combination of PGK1 and CXCR4 expression levels and disease-free interval (DFI) survival from TCGA KIRC objects. D PGK1 induced the CXCR4-mediated phosphorylation of AKT (p-AKT) and ERK (p-ERK), and blockade of CXCR4 signaling by AMD3100 treatment did not alter cellular PGK1 expression in KIRC cells. E PGK1 knockdown inhibited cell proliferation and decreased glucose consumption and lactate production in OS-RC-2 cells. The darker the color develops, the more glucose remaining and lactate produced. F CXCR4, p-AKT, and p-ERK were decreased by PGK1 inhibition in 786-O and OS-RC-2 cells. G Protein levels of PGK1, CXCR4, p-AKT, and p-ERK were detected in xenograft tumors inoculating 786-O^-PGK1 cells. β-actin served as the internal control. Glycolysis suppression by 40 μM WZB117 treatment for 48 h significantly downregulated CXCR4 and p-ERK (H) and reduced glucose consumption and lactate production (I) in RCC cells.