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. 2021 May 14;40:168. doi: 10.1186/s13046-021-01933-7

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© The Author(s) 2021

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. 6 — Creatine reduces mitochondrial activity and oxygen consumption, and mitigates ROS production in hypoxic TNBC cells. shNC and shSlc6a8#2 (shSlc) MDA-MB-231 and BT549 cells were cultured under normoxia and hypoxia, and administered 5 mM creatine or PBS, then mitochondrial activity, oxygen consumption and ROS products were assessed. a Mitochondrial membrane potential was determined by JC-1 staining. b, c Mitochondrial complex I and III activities were measured using reagent kit, as elaborated in methods. d, e Oxygen consumption rate (OCR) and basal respiration (complex I mediated OCR) were detected using a Seahorse XF24 Extracellular Flux Analyzer. f ROS level was measured by DCFH-DA staining. Data were presented as mean ± SD (^*P < 0.05, ^**P < 0.01, ^***P < 0.001, ns means no statistical difference)