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. 2023 May 6;42(25):2047–2060. doi: 10.1038/s41388-023-02704-8

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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. 9 — The expression of ALKBH5 was increased under hypoxic conditions which led to increased stability of HDAC4 mRNA via m6A modification and in a YTHDF2 dependent manner. Increased HDAC4 enhanced HIF1a protein stability. And then overexpressed HIF1a promoted transcription of ALKBH5, LDHA, HK2, GLUT1 and GLUT3. Therefore, ALKBH5/HDAC4/HIF1α form a positive feedback loop, which then induces a more glycolytic metabolism and migration of PC cells under hypoxia.