{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"submitter":["Nickols NG"],"pagination":["561-571"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-ECPF-GEOD-7835"],"project":["EurocanPlatform"],"abstract":["Transcription mediated by hypoxia inducible factor (HIF-1) contributes to tumor angiogenesis and metastasis but is also involved in the activation of cell-death pathways and normal physiological processes.  Given the complexity of HIF-1 signaling it could be advantageous to target a subset of HIF-1 effectors rather than the entire pathway.  We compared the genome-wide effects of three molecules that each interfere with the HIF-1-DNA interaction: a polyamide targeted to the hypoxia response element (HRE), siRNA targeted to HIF-1α, and echinomycin, a DNA binding natural product with a similar but less specific sequence preference to the polyamide.  The polyamide affects a subset of hypoxia-induced genes that are consistent with the binding site preferences of the polyamide.  For comparison, siRNA targeted to HIF-1α and echinomycin each affect the expression of nearly every gene induced by hypoxia.  Remarkably, the total number of genes affected by either polyamide or HIF-1α siRNA over a range of thresholds is comparable.  The data shows how polyamides can be used to affect a subset of a pathway regulated by a transcription factor.  In addition, this study offers a unique comparison of three complementary approaches towards exogenous control of endogenous gene expression. Experiment Overall Design: Hypoxia-mimetic DFO (deferoxamine)-stimulated U251 cells that were treated with polyamide 1, HIF-1α siRNA, and echinomycin were compared to control cells that were also DFO-stimulated.  Cells not stimulated with DFO were also compared to the DFO-stimulated controls.  Three biological replicates were included for each treatment/condition."],"repository":["biostudies-other"],"experiment_type":["transcription profiling by array"],"data_source":["EurocanPlatform"],"omics_type":["Unknown"],"volume":["2"],"journal":["ACS chemical biology"],"species":["Homo sapiens"],"pubmed_authors":["Farkas ME","Nickols NG","Jacobs CS","Dervan PB"],"additional_accession":[]},"is_claimable":false,"name":"Transcription profiling by array of human glioblastoma cells after stimulation with deferoxamine and treatment with polyamide 1, echinomycin, or HIF-1a siRNA","description":"Transcription mediated by hypoxia inducible factor (HIF-1) contributes to tumor angiogenesis and metastasis but is also involved in the activation of cell-death pathways and normal physiological processes.  Given the complexity of HIF-1 signaling it could be advantageous to target a subset of HIF-1 effectors rather than the entire pathway.  We compared the genome-wide effects of three molecules that each interfere with the HIF-1-DNA interaction: a polyamide targeted to the hypoxia response element (HRE), siRNA targeted to HIF-1α, and echinomycin, a DNA binding natural product with a similar but less specific sequence preference to the polyamide.  The polyamide affects a subset of hypoxia-induced genes that are consistent with the binding site preferences of the polyamide.  For comparison, siRNA targeted to HIF-1α and echinomycin each affect the expression of nearly every gene induced by hypoxia.  Remarkably, the total number of genes affected by either polyamide or HIF-1α siRNA over a range of thresholds is comparable.  The data shows how polyamides can be used to affect a subset of a pathway regulated by a transcription factor.  In addition, this study offers a unique comparison of three complementary approaches towards exogenous control of endogenous gene expression. Experiment Overall Design: Hypoxia-mimetic DFO (deferoxamine)-stimulated U251 cells that were treated with polyamide 1, HIF-1α siRNA, and echinomycin were compared to control cells that were also DFO-stimulated.  Cells not stimulated with DFO were also compared to the DFO-stimulated controls.  Three biological replicates were included for each treatment/condition.","dates":{"release":"2016-04-14T14:43:35Z","publication":"2007 Aug","modification":"2016-04-14T14:43:35Z","creation":"2016-04-14T14:43:35Z"},"accession":"S-ECPF-GEOD-7835","cross_references":{"GEO":["GSE7835"],"ArrayExpress":["E-GEOD-7835"],"EFO":["EFO_0000322","EFO_0000519"],"ArrayExpress files":["E-GEOD-7835"]}}