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. 2023 Jan 2;42:1. doi: 10.1186/s13046-022-02574-0

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© The Author(s) 2022

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. 8 — Proposed model for PKM2 regulation by ENO2 in HNSCC cells. ENO2 binds to PKM2 to prevent PKM2 protein degradation by the ubiquitin-proteasome system and facilitates the nuclear translocation of PKM2 by mediating AKT phosphorylation, potentiating PKM2-mediated glycolytic flux and CCND1-associated cell cycle progression