Abstract
There are many approaches used to control breast cancer, although the most efficient strategy is the reactivation of apoptosis. Since mitochondria play an important role in cellular metabolism and homeostasis, as well as in the regulation of cell death pathways, we focus here on metabolic remodeling and mitochondrial alterations present in breast tumor cells. We review strategies including classes of compounds and delivery systems that target metabolic and specific mitochondrial alterations to kill tumor cells without affecting their normal counterparts. We present here the arguments for the improvement of already existent molecules and the design of novel promising anticancer drug candidates that target breast cancer mitochondria.
Acknowledgements
We are extremely grateful to Alexandra Holy (Mills College, Oakland, CA, USA) for English proofreading.
Financial & competing interests disclosure
Work in the authors’ laboratory is performed with funding from the Portuguese Foundation for Science and Technology (FCT) co-funded by COMPETE/FEDER (PTDC/SAU-TOX/117912/2010, PTDC/QUI-QUI/101409/2008, and PEst-C/SAU/LA0001/2013–2014). TL Serafim is supported by a Post-Doctoral fellowship from the FCT (SFRH/BPD/75959/2011). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
No writing assistance was utilized in the production of this manuscript.