Role of mitochondria in rescuing glycolytically inhibited subpopulation of triple negative but not hormone-responsive breast cancer cells
Autor: | Asmaa Reda, Ahmed A. Abd-Rabou, Sameh S. Ali, Ali M. Mahmoud, Salwa Sabet, Mohamed Adel, Alaa Refaat |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: |
Cell Survival
Population lcsh:Medicine Apoptosis Triple Negative Breast Neoplasms Oxidative phosphorylation Mitochondrion medicine.disease_cause Article Oxidative Phosphorylation PARP1 Breast cancer Cell Line Tumor medicine Humans Viability assay education lcsh:Science Glyceraldehyde 3-phosphate dehydrogenase education.field_of_study Multidisciplinary biology Chemistry Cell Cycle lcsh:R Energy metabolism Mitochondria biology.protein Cancer research MCF-7 Cells Female lcsh:Q Neoplasm Recurrence Local Carcinogenesis Glycolysis |
Zdroj: | Scientific Reports, Vol 9, Iss 1, Pp 1-15 (2019) Scientific Reports |
ISSN: | 2045-2322 |
DOI: | 10.1038/s41598-019-50141-z |
Popis: | Triple-negative breast cancer (TNBC) subtype is among the most aggressive cancers with the worst prognosis and least therapeutic targetability while being more likely to spread and recur. Cancer transformations profoundly alter cellular metabolism by increasing glucose consumption via glycolysis to support tumorigenesis. Here we confirm that relative to ER-positive cells (MCF7), TNBC cells (MBA-MD-231) rely more on glycolysis thus providing a rationale to target these cells with glycolytic inhibitors. Indeed, iodoacetate (IA), an effective GAPDH inhibitor, caused about 70% drop in MDA-MB-231 cell viability at 20 μM while 40 μM IA was needed to decrease MCF7 cell viability only by 30% within 4 hours of treatment. However, the triple negative cells showed strong ability to recover after 24 h whereas MCF7 cells were completely eliminated at concentrations |
Databáze: | OpenAIRE |
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