ArticleCancer biology & therapy2009
Mitochondrial electron transport chain blockers enhance 2-deoxy-D-glucose induced oxidative stress and cell killing in human colon carcinoma cells.
Article in Cancer biology & therapy, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 69 citations in OpenAlex.
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- Antipsychotic Drug Cariprazine Induces Distinct Cell Death Mechanisms in HeLa and HCT116 Cells as a Potential Inhibitor of Qi-Site of Cytochrome bc1 Reductase.Biomedicines · 2026Article
- Targeting mitochondria as a potential therapeutic strategy against radioresistance in cancer.Frontiers in oncology · 2026Review
- Reactive oxygen species (ROS) in cancer: from redox signaling and metabolic plasticity to therapeutic vulnerabilities.Exploration of targeted anti-tumor therapy · 2026Review
- Reinventing Radiobiology in the Light of FLASH Radiotherapy.Annual review of cancer biology · 2023Article
- Metabolic reprogramming in renal cancer: Events of a metabolic disease.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- Rotenone restrains the proliferation, motility and epithelial-mesenchymal transition of colon cancer cells and the tumourigenesis in nude mice via PI3K/AKT pathway.Clinical and experimental pharmacology & physiology · 2020Article
- The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21Biomolecules · 2020Article
- Redox Homeostasis and Metabolism in Cancer: A Complex Mechanism and Potential Targeted Therapeutics.International journal of molecular sciences · 2020Review
- A synthetic lethal drug combination mimics glucose deprivation-induced cancer cell death in the presence of glucose.The Journal of biological chemistry · 2020Article
- S100A4 alters metabolism and promotes invasion of lung cancer cells by up-regulating mitochondrial complex I protein NDUFS2.The Journal of biological chemistry · 2019Article
- Redox Paradox: A Novel Approach to Therapeutics-Resistant Cancer.Antioxidants & redox signaling · 2018Review
- Biological and metabolic effects of IACS-010759, an OxPhos inhibitor, on chronic lymphocytic leukemia cells.Oncotarget · 2018Article
- Article
- Absence of REV3L promotes p53-regulated cancer cell metabolism in cisplatin-treated lung carcinoma cells.Biochemical and biophysical research communications · 2018Article
- Synthesis and in vitro biological evaluation of thiosulfinate derivatives for the treatment of human multidrug-resistant breast cancer.Acta pharmacologica Sinica · 2017Article
- D-penicillamine combined with inhibitors of hydroperoxide metabolism enhances lung and breast cancer cell responses to radiation and carboplatin via HFree radical biology & medicine · 2017Article
- ID2 promotes survival of glioblastoma cells during metabolic stress by regulating mitochondrial function.Cell death & disease · 2017Article
- Synergistic Anticancer Action of Lysosomal Membrane Permeabilization and Glycolysis Inhibition.The Journal of biological chemistry · 2016Article
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6 authors at 1 institution in 1 country.
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Abstract
Increasing evidence suggests that cancer cells (relative to normal cells) have altered mitochondrial electron transport chains (ETC) that are more likely to form reactive oxygen species (ROS; i.e., O(2)(*-) and H(2)O(2)) resulting in a condition of chronic metabolic oxidative stress, that maybe compensated for by increasing glucose and hydroperoxide metabolism. In the current study, the ability of an inhibitor of glucose metabolism, 2-deoxy-D-glucose (2DG), combined with mitochondrial electron transport chain blockers (ETCBs) to enhance oxidative stress and cytotoxicity was determined in human colon cancer cells. Treatment of HT29 and HCT116 cancer cells with Antimycin A (Ant A) or rotenone (Rot) increased carboxy-dichlorodihydrofluorescein diacetate (H2DCFDA) and dihydroethidine (DHE) oxidation, caused the accumulation of glutathione disulfide and enhanced 2DG-induced cell killing. In contrast, Rot did not enhance the toxicity of 2DG in normal human fibroblasts supporting the hypotheses that cancer cells are more susceptible to inhibition of glucose metabolism in the presence of ETCBs. In addition, 2-methoxy-antimycin A (Meth A; an analog of Ant A that does not have ETCB activity) did not enhance 2DG-induced DHE oxidation or cytotoxicity in cancer cells. Finally, in HT29 tumor bearing mice treated with the combination of 2DG (500 mg/kg) + Rot (2 mg/kg) the average rate of tumor growth was significantly slower when compared to control or either drug alone. These results show that 2DG-induced cytotoxicity and oxidative stress can be significantly enhanced by ETCBs in human colon cancer cells both in vitro and in vivo.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.