2017
DOI: 10.18632/aging.101304
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Abstract: Here, we used MCF7 cells as a model system to interrogate how MYC/RAS co-operativity contributes to metabolic flux and stemness in breast cancer cells. We compared the behavior of isogenic MCF7 cell lines transduced with c-Myc or H-Ras (G12V), either individually or in combination. Cancer stem cell (CSC) activity was measured using the mammosphere assay. c-Myc augmented both mammosphere formation and mitochondrial respiration, without any effects on glycolytic flux. In contrast, H-Ras (G12V) synergistically au… Show more

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Cited by 15 publications
(11 citation statements)
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References 26 publications
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“…Cancer stem cells in breast cancer have two different forms, the mesenchymal-like cancer stem cells are CD44+/CD24−, while the epithelial-like cancer stem cells are aldehyde dehydrogenase 1 family, member A1 (ALDH1) positive [89,90]. The inhibition of mitochondrial oxidation can increase the proportions of cancer stroma to stem cells, facilitating the efficiency of conventional chemotherapy that primarily targets stromal cells [86,91,92,93]. Larger proportions of stem cells than ER+ positive cancers characterize TNBCs [82,83].…”
Section: The Dysregulation Of Metabolism In Breast Cancermentioning
confidence: 99%
“…Cancer stem cells in breast cancer have two different forms, the mesenchymal-like cancer stem cells are CD44+/CD24−, while the epithelial-like cancer stem cells are aldehyde dehydrogenase 1 family, member A1 (ALDH1) positive [89,90]. The inhibition of mitochondrial oxidation can increase the proportions of cancer stroma to stem cells, facilitating the efficiency of conventional chemotherapy that primarily targets stromal cells [86,91,92,93]. Larger proportions of stem cells than ER+ positive cancers characterize TNBCs [82,83].…”
Section: The Dysregulation Of Metabolism In Breast Cancermentioning
confidence: 99%
“…ROS bind to proteins to generate carbonyl derivatives[ 62 ], alter the tertiary structure of the proteins, and promote protein/DNA[ 63 ]-protein cross-linking, leading to changes in the protein activity of CSC marker proteins such as octamer binding transcription factor 4 and sex determining region Y box 2 (Sox2)[ 64 ]. ROS directly attack DNA bases and easily cause deoxyguanosine modifications to one carbon atom (that is, 8-OHdG)[ 62 ], which may be one of the causes of point mutations in proto-oncogenes or tumor suppressor genes, such as Ras and p53[ 65 , 66 ]. Free radicals generate lipid peroxides through oxidation, which can damage cell membranes and promote ferroptosis.…”
Section: Impact Of Ros From Pdt On Cscsmentioning
confidence: 99%
“…Doxycycline functionally behaves as a non-toxic inhibitor of mitochondrial biogenesis, because of the evolutionarily conserved similarities between bacterial ribosomes and mitochondrial ribosomes ( 10 12 ). Therefore, this “manageable side-effect” of doxycycline could be repurposed as a “therapeutic effect,” to target and inhibit mitochondrial biogenesis in CSCs ( 13 , 14 ).…”
Section: Introductionmentioning
confidence: 99%