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. 2022 Oct 4;13(10):848. doi: 10.1038/s41419-022-05299-2

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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 After adding 5AZ, Bobcat339, DZNEP, TSA, or SAHA to AGS and HGC-27 cells, the mRNA expression changes in CRABP2 were detected. The methylation (b) and hydroxymethylation (c) levels of OXA-resistant GC cells and parental GC cells were examined. d The expression and activity of DNA methylase, demethylase, and hydroxymethylase from OXA-resistant and parental GC cells were examined by western blotting. e The activity of hydroxymethylase TET1 was detected in OXA-resistant GC cells and parental GC cells. f Schematic diagram of the predicted and designed methylation sites in the promoter region of CRABP2. g ChIP experiments using a TET1 antibody were performed in OXA-resistant GC cells. h Hydroxymethylated ChIP assays were performed in OXA-resistant GC cells. After knocking down or overexpressing TET1 in OXA-resistant GC cells, the expression of CRABP2 was examined by qRT–PCR (i) and western blotting (j). *P < 0.05, **P < 0.01, ***P < 0.001, ns not significant.