A mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis and inhibits cancer growth.

By S. Bonnet, S. Archer, J. Allalunis-Turner, A. Haromy, C. Beaulieu, Richard B. Thompson, Christopher T. Lee, G. Lopaschuk, L. Puttagunta, Sandra N. Bonnet and 6 more. Cancer Cell, 2007

1,563 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9b9adbbeab192f79dd6df3ce9322391abcd3a6c4

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Environment impacts the metabolic dependencies of Ras-driven non-small cell lung cancer (2016, background): “…conversion in tumors (Warburg effect) (Keshari et al., 2013; Rodrigues et al., 2014), but understanding the metabolic phenotype of cancer is based mostly on cell culture studies, including the idea that glucose oxidation in the TCA cycle is limited (Bonnet et al., 2007; Cairns et al., 2011).”
Mechanisms of disease: pulmonary arterial hypertension (2011, background): “168 Studies of this drug in several experimental models of pulmonary hypertension have also been encouraging.”
Dichloroacetate (DCA) as a potential metabolic-targeting therapy for cancer (2008, background): “…to the induction of apoptosis by DCA in non-small cell lung cancer, breast cancer and glioblastoma cell lines reported in our original publication (Bonnet et al, 2007), very recently DCA was shown to induce apoptosis in endometrial (Wong et al, 2008) and prostate (Cao et al, 2008) cancer cells by…”
Blinded by the Light: The Growing Complexity of p53. (2009, background): “Indeed, the dependence of cancers on metabolic transformation is highlighted by mouse models of cancer in which interfering with these altered metabolic programs profoundly limits tumor cell growth (Bonnet et al., 2007; Christofk et al., 2008; Fantin et al., 2006).”
HIF-1 mediates metabolic responses to intratumoral hypoxia and oncogenic mutations. (2013, neutral): “When DCA was administered in the drinking water of athymic rats bearing subcutaneous xenografts of A549 human lung cancer cells, xenograft growth was significantly inhibited (103).”
Cancer cell metabolism: Warburg and beyond. (2008, background): “Intriguingly, Bonnet et al. (2007) have reported that treating cancer cells with dichloroacetate (DCA), a small molecule inhibitor of pyruvate dehydrogenase kinase, has striking effects on their survival and on xenograft tumor growth.”
The Warburg effect in tumor progression: Mitochondrial oxidative metabolism as an anti-metastasis mechanism (2014, background): “This metabolic normalization increases mitochondrial respiration and ROS generation, and induces apoptosis in certain cancer cells even under attached conditions [89] [90].”
Hypoxia-inducible factors: mediators of cancer progression and targets for cancer therapy (2012, background): “Fifth, HIF-1-dependent metabolic reprogramming [16, 17, 30, 44, 45, 87, 88] may decrease ROS levels and thereby inhibit chemotherapy-induced cell death [89].”
Metabolic Modulation of Glioblastoma with Dichloroacetate (2010, neutral): “9445–9450 (2007).”
Cisplatin Induces a Mitochondrial-ROS Response That Contributes to Cytotoxicity Depending on Mitochondrial Redox Status and Bioenergetic Functions (2013, methodology): “To validate our prediction we used the pyruvate dehydrogenase kinase inhibitor dichloroacetate (DCA) to switch the metabolism of cancer cells from glycolysis to glucose oxidation [44].”
Mitochondria in cancer cells: what is so special about them? (2008, neutral): “As a result, such treatmentdecreased mitochondrial membrane potential (DC) and increased mitochondrial production of ROS in cancer cells, but not in normal cells [ 74 ].”