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. 2020 May 7;10:7714. doi: 10.1038/s41598-020-64880-x

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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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Vitamin K2 promotes glycolysis and inhibits TCA cycle in bladder cancer cells. (A–D) Vitamin K2 time or dose-dependently affected the glucose consumption and lactate production in bladder cancer T24 and EJ cells. (E) and (F) Western blot showed the effect of 50 μM Vitamin K2 on the expression of glycolytic proteins or enzymes in bladder cancer T24 and EJ cells. (G) T24 cells were exposed to 50 μM Vitamin K2 for 12 hours and the quantitative analysis of Acetyl-CoA amount was measured by LC-MS. (H) Western blot showed the effect of 50 μM Vitamin K2 on the phosphorylation of PDH in T24 cells. (I) and (J) T24 cells were exposed to 50 μM Vitamin K2 for 12 hours and the quantitative analysis of the metabolites content in TCA cycle was measured by LC-MS. Data are presented as the mean ± SD of at least three independent experiments. *P < 0.05, **P < 0.01 and ***P < 0.001.