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. 2024 Mar 13;24:59. doi: 10.1186/s12894-024-01444-5

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© The Author(s) 2024

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — PFK-1 suppressed the histone lactylation of BC cells and ZEB1 transcriptional activity. After sh-PFK-1 transfection and LA treatment, (A) the expression of pan-kla and H3K18la was measured by western blot. (B, C) ChIP assay showed that PFK-1 knockdown inhibited the binding of H3K18 with the promoter of ZEB1. (D, E) Luciferase assay further indicated that PFK-1 knockdown suppressed the transcription activity of ZEB1. Sh-PFK-1 transfection decreased the mRNA (F-G) and protein (H) level of ZEB1ZEB1 mRNA expression in UM-UC-1 and RT112 cell lines