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. 2023 May 18;23:160. doi: 10.1186/s12906-023-03975-0

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© The Author(s) 2023

Open AccessThis 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. 4 — H3K27me3 related cantharidin treatment target prediction analysis in HCC. (A) Venn diagram shows the genes of liver carcinoma and H3K27me3 related cantharidin treatment targets. (B) The expression of these targets in LIHC. Red represents high expression; blue represents low expression. P < 0.05 is considered significant. (C) Proteins expression of significantly up-regulated genes in LIHC. (D) These genes expression in cantharidin treated HepG2 cell. The * P < 0.05 was regarded as statistically significant. (E) H3K27me3 is dramatically enriched in these genes promoters based on the ChIP-seq results in HepG2