{"database":"EGA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"dataset_type":["Illumina ChIP-Sequencing"],"full_dataset_link":["https://ega-archive.org/datasets/EGAD00010000859"],"sample_count":["16"],"description":["EGA dataset EGAD00010000859"],"repository":["EGA"],"title":["SmadChip"],"pubmed_abstract":["The transforming growth factor beta (TGF-β) signaling pathway exerts opposing effects on cancer cells, acting as either a tumor promoter or a tumor suppressor. Here, we show that these opposing effects are a result of the synergy between SMAD3, a downstream effector of TGF-β signaling, and the distinct epigenomes of breast-tumor-initiating cells (BTICs). These effects of TGF-β are associated with distinct gene expression programs, but genomic SMAD3 binding patterns are highly similar in the BTIC-promoting and BTIC-suppressing contexts. Our data show cell-type-specific patterns of DNA and histone modifications provide a modulatory layer by determining accessibility of genes to regulation by TGF-β/SMAD3. LBH, one such context-specific target gene, is regulated according to its DNA methylation status and is crucial for TGF-β-dependent promotion of BTICs. Overall, these results reveal that the epigenome plays a central and previously overlooked role in shaping the context-specific effects of TGF-β in cancer."],"pubmed_title":["Context-Specific Effects of TGF-β/SMAD3 in Cancer Are Modulated by the Epigenome."],"pubmed_authors":["Tufegdzic Vidakovic Ana A, Rueda Oscar M OM, Vervoort Stephin J SJ, Sati Batra Ankita A, Goldgraben Mae Akilina MA, Uribe-Lewis Santiago S, Greenwood Wendy W, Coffer Paul J PJ, Bruna Alejandra A, Caldas Carlos C"],"additional_accession":[]},"is_claimable":false,"name":"SmadChip","description":"Smad3 ","dates":{"updated":"2018-07-18 09:50:57"},"accession":"EGAD00010000859","cross_references":{"TAXONOMY":["9606"],"pubmed":["26686634"],"EGA":["EGAC00001000407","EGAS00001001570"]}}