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. 2021 Aug 6;10(8):58. doi: 10.1038/s41389-021-00347-6

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© The Author(s) 2021

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 — The elevated levels of transcriptional activator E2F1 and gain of 5hmC marks on the ESRP1 promoter govern the ESRP1 upregulation. However, ESRP1 expression is severely diminished within the hypoxic tumor niche despite a high E2F1 level. Mechanistically, hypoxia-driven reduction in TET3 activity coerces the E2F1 binding site on the ESRP1 promoter to lose 5hmC marks while gaining DNMT3A/3B-dependent 5mC marks. Additionally, elevated E2F1 regulates the hypoxia-specific spliceome by inducing SRSF7 expression.