Unknown,Transcriptomics,Genomics,Proteomics

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Altering cancer transcriptomes using epigenomic inhibitors [RNA-Seq]


ABSTRACT: We have compared the genome-wide effects on the transcriptome after treatment with ICG-001 (the specific CBP inhibitor) versus C646, a compound that competes with acetyl-coA for the Lys-coA binding pocket of both CBP and p300. We found that both drugs cause large-scale changes in the transcriptome of HCT116 colon cancer cells and PANC1 pancreatic cancer cells, and reverse some tumor-specific changes in gene expression. Interestingly, although the epigenetic inhibitors affect cell cycle pathways in both the colon and pancreatic cancer cell lines, the WNT signaling pathway was affected only in the colon cancer cells. Notably, WNT target genes were similarly down-regulated after treatment of HCT116 with C646 as with ICG-001. To identify genes affected by direct targeting of a component of the transcriptional complex implicated in WNT regulation, we used siRNAs to knockdown TCF7L2 in PANC1 cells. Cells were treated with control siRNAs or siRNAs specific for TCF7L2 and RNA was analyzed by RNA-seq.

ORGANISM(S): Homo sapiens

SUBMITTER: Seth Frietze 

PROVIDER: E-GEOD-63776 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Altering cancer transcriptomes using epigenomic inhibitors.

Gaddis Malaina M   Gerrard Diana D   Frietze Seth S   Farnham Peggy J PJ  

Epigenetics & chromatin 20150224


<h4>Background</h4>Due to the hyper-activation of WNT signaling in a variety of cancer types, there has been a strong drive to develop pathway-specific inhibitors with the eventual goal of providing a chemotherapeutic antagonist of WNT signaling to cancer patients. A new category of drugs, called epigenetic inhibitors, are being developed that hold high promise for inhibition of the WNT pathway. The canonical WNT signaling pathway initiates when WNT ligands bind to receptors, causing the nuclear  ...[more]

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