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. 2021 Jan 13;14:7. doi: 10.1186/s13072-020-00380-6

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© The Author(s) 2021

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 — Functional annotation of significant DMRs reveals differential methylation at alternative MAP2K3 exons leading to coordinated MKK3 expression. a KEGG pathway analysis of CNF and PNF methylation profiles confirms that multiple pathways are regulated epigenetically including growth factor, inflammatory, pain signaling and oxytocin pathways. b, c Differential methylation was observed in upstream regulatory sites in MAP2K3 that control alternative leading exon expression. d Western blot analysis of MKK3 protein (actin loading control). Beta-values for tumor-type DMRs (DMR1/DMR2) shown below. e DMR1 beta-values correlate strongly with MKK3/Actin ratio expression values (p < 0.01; = − 0.846)