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. 2020 Sep 11;9(9):81. doi: 10.1038/s41389-020-00265-z

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© The Author(s) 2020

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. 8 — In ECSCs, HIF-1α and HIF-2α activate the expression of ALKBH5 under hypoxic conditions, facilitating SOX2 expression via demethylation of SOX2 mRNA. However, knockdown of HIF-1α and HIF-2α inhibits ALKBH5 and prevents the stem-like state of ECSCs, which is reversed by exposure to hypoxia or ALKBH5 overexpression. Blocking HIFs with KC7F2 inhibits the HIF/ALKBH5/SOX2 axis, which reduces the stemness of ECSCs, while activating HIFs with CoCl₂ maintains an ECSC stem-like state. Collectively, hypoxia promotes the expression of the demethylase ALKBH5 and decreases m⁶A SOX2 by inducing demethylation of SOX2 mRNA, thus promoting the expression of SOX2 and the stemness of ECSCs.