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. 2023 Dec 11;14(12):815. doi: 10.1038/s41419-023-06352-4

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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. 8 — TNBC predominantly relies on glycolysis-mediated ATP production in tumors with limited oxygen and nutrients. Remarkably, Mint3 depletion affects glycolysis-mediated ATP production and activates AMPK, resulting in decreased HSF-1 Ser326 phosphorylation and HSP70 expression. The ensuing reduction in HSP70 levels sensitizes TNBC tumors to chemotherapy. Conversely, TNBC cells cultured under conditions of ample oxygen and nutrient availability exhibit a reduced dependency on glycolysis-mediated ATP production. Consequently, Mint3 depletion fails to exert an impact on AMPK activity or HSP70 expression, resulting in comparable chemoresistance in TNBC cells.