{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"submitter":["Bonnet S"],"pagination":["37-51"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-ECPF-GEOD-6014"],"project":["EurocanPlatform"],"abstract":["The unique metabolic profile of most cancers (aerobic glycolysis) might confer apoptosis-resistance and be therapeutically targeted. Compared to normal cells, several human cancers have high mitochondrial membrane potential and low expression of the K+ channel Kv1.5, both contributing to apoptosis-resistance. Dichloroacetate (DCA), an inhibitor of the mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases mitochondrial membrane potential, increases mitochondrial-H2O2 and activates Kv channels in all cancer, but not normal cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism. DCA induces apoptosis, decreases proliferation and tumor growth in vitro and in vivo, without apparent toxicity. Molecular inhibition of PDK2 by siR"],"repository":["biostudies-other"],"experiment_type":["transcription profiling by array"],"data_source":["EurocanPlatform"],"omics_type":["Unknown"],"volume":["11"],"journal":["Cancer cell"],"species":["Homo sapiens"],"pubmed_authors":["Lopaschuk GD","Harry G","Lee CT","Haromy A","Thebaud B","Allalunis-Turner J","Puttagunta L","Thompson R","Andrade MA","Porter CJ","Michelakis ED","Bonnet S","Beaulieu C","Archer SL","Hashimoto K"],"additional_accession":[]},"is_claimable":false,"name":"Transcription profiling of lung carcinoma and brain glioblastoma cells were analalyzed, with microarrays run both for control and treatment with dichloroacetate reveals a mitochondria-K+ channel axis is suppressed in cancer and its normalization promotes apoptosis inhibits cancer growth","description":"The unique metabolic profile of most cancers (aerobic glycolysis) might confer apoptosis-resistance and be therapeutically targeted. Compared to normal cells, several human cancers have high mitochondrial membrane potential and low expression of the K+ channel Kv1.5, both contributing to apoptosis-resistance. Dichloroacetate (DCA), an inhibitor of the mitochondrial pyruvate dehydrogenase kinase (PDK), shifts metabolism from glycolysis to glucose oxidation, decreases mitochondrial membrane potential, increases mitochondrial-H2O2 and activates Kv channels in all cancer, but not normal cells; DCA upregulates Kv1.5 by an NFAT1-dependent mechanism. DCA induces apoptosis, decreases proliferation and tumor growth in vitro and in vivo, without apparent toxicity. Molecular inhibition of PDK2 by siR","dates":{"release":"2016-04-14T14:38:51Z","publication":"2007 Jan","modification":"2016-04-14T14:38:51Z","creation":"2016-04-14T14:38:51Z"},"accession":"S-ECPF-GEOD-6014","cross_references":{"GEO":["GSE6014"],"ArrayExpress":["E-GEOD-6014"],"EFO":["EFO_0000322","EFO_0000519","EFO_0001071"],"ArrayExpress files":["E-GEOD-6014"]}}