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. 2019 Sep 24;9:13748. doi: 10.1038/s41598-019-50141-z

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© The Author(s) 2019

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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Schematic representation of the mechanism of IA-induced cell death in MCF7 cells and the role of mitochondria in rescuing MDA-MB-231 cells under the same treatment. Our analyses showed that basal respiratory activity in MCF7 cells were remarkably higher than MDA-MB-231 while the later showed higher glycolytic activities. However, multiple converging evidence from the current work revealed that mitochondria of MDA-MB-231 cells were more coupled (less proton leak) and possess remarkably greater spare respiratory capacity than hormone responsive MCF7 cells. Moreover, MCF7 cells exhibit significantly higher non-mitochondrial oxygen consumption which might be attributable to cell surface oxygen consumption as mediated by trans-plasma membrane electron-transport (t-PMET). It is conceivable that increased cellular levels of NAD⁺ either through enhanced mitochondrial and/or t-PMET activities may explain increased PARP-1 levels leading to augmented DNA repair mechanism in treated TNBC cells. Moreover, the lack of respiratory reserve capacity in MCF7 cells implies that these cells are relatively less competent in handling bioenergetic stress which is reflected in increased apoptosis, lowered DNA repair, and cell cycle arrest leading to effective cell death.