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. 2023 Feb 17;8:69. doi: 10.1038/s41392-023-01341-7

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© The Author(s) 2023

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. 3 — The roles of different epigenetic modifications in tumor resistance. DNA methylation is co-regulated by DNA methyltransferases and DNA demethylases, mainly influencing apoptosis, stemness, EMT, and cell proliferation through Notch and Wnt/β-catenin signaling pathways to modulate drug resistance. Non-coding RNAs mainly include four small nucleotides and two large nucleotides, which promote or inhibit tumor resistance. Similarly, histone methylation and acetylation are histone modifications. They keep gene expressions in balance through histone demethylases and methyltransferases, histone acetyltransferases and histone deacetylases, respectively, and function as a double-edged sword in cancer resistance