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- W2890250729 abstract "Breast cancer cells have different requirements on metabolic pathways in order to sustain their growth. Triple negative breast cancer (TNBC), an aggressive breast cancer subtype relies mainly on glycolysis, while estrogen receptor positive (ER+) breast cancer cells possess higher mitochondrial oxidative phosphorylation (OXPHOS) levels. However, breast cancer cells generally employ both pathways to sustain their metabolic needs and to compete with the surrounding environment. In this study, we demonstrate that the mitochondrial fission inhibitor MDIVI-1 alters mitochondrial bioenergetics, at concentrations that do not affect mitochondrial morphology. We show that this effect is accompanied by an increase in glycolysis consumption. Dual targeting of glycolysis with 2-deoxy-D-glucose (2DG) and mitochondrial bioenergetics with MDIVI-1 reduced cellular bioenergetics, increased cell death and decreased clonogenic activity of MCF7 and HDQ-P1 breast cancer cells. In conclusion, we have explored a novel and effective combinatorial regimen for the treatment of breast cancer." @default.
- W2890250729 created "2018-09-27" @default.
- W2890250729 creator A5041419076 @default.
- W2890250729 creator A5066581807 @default.
- W2890250729 creator A5090895071 @default.
- W2890250729 date "2018-09-11" @default.
- W2890250729 modified "2023-10-16" @default.
- W2890250729 title "Metabolic Targeting of Breast Cancer Cells With the 2-Deoxy-D-Glucose and the Mitochondrial Bioenergetics Inhibitor MDIVI-1" @default.
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- W2890250729 doi "https://doi.org/10.3389/fcell.2018.00113" @default.
- W2890250729 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6141706" @default.
- W2890250729 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30255019" @default.
- W2890250729 hasPublicationYear "2018" @default.
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