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CREBBP/EP300 acetyltransferase inhibition targets lineage specific enhancers to inhibit the proliferation of ER+ breast cancer cells [ChIP-Seq]

ABSTRACT: MCF7 were treated with a CREBBP/EP300 acetyltransferase inhibitor CPI-1612 or DMSO and ChIP-seq was performed for H3K27ac and H3K9ac.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190161 | GEO | 2022/03/04

REPOSITORIES: GEO

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CREBBP/EP300 acetyltransferase inhibition targets lineage specific enhancers to inhibit the proliferation of ER+ breast cancer cells [ATAC-Seq]

Project description:MCF7 cells were treated with a CREBBP/EP300 acetyltransferase inhibitor CPI-1612 and chromatin status was measured via ATAC-seq

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CREBBP/EP300 acetyltransferase inhibition targets lineage specific enhancers to inhibit the proliferation of ER+ breast cancer cells [scATAC-Seq]

Project description:MCF7 cells were treated with a CREBBP/EP300 acetyltransferase inhibitor CPI-1612 and chromatin status was measured via single-cell ATAC-seq

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CREBBP/EP300 acetyltransferase inhibition targets lineage specific enhancers to inhibit the proliferation of ER+ breast cancer cells [RNA-Seq]

Project description:MCF7, T47D, or ZR751 cells were treated with a CREBBP/EP300 acetyltransferase inhibitor CPI-1612 and/or Fulvestrant and expression changes were measured via RNA-seq

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Expression data from WT, Crebbp+/- and Ep300+/- bone marrow stroma

Project description:We found that the bone marrow microenvironment of Crebbp+/- mice was unable to properly maintain the immature stem - and progenitor pools. Instead, it stimulates myeloid differentiation that progresses into a myeloproliferative-like disease. Since CREBBP is a transcriptional co-activator, we used gene expression analysis to globally assess functional deficiencies in Crebbp+/- bone marrow stroma cells at a molecular level. Ep300 encodes a protein which is highly similar in structure and function to CREBBP; nevertheless, Ep300+/- mice suffer neither excessive myeloid differentiation nor loss of HSCs. Therefore, to identify expression changes specifically related to Crebbp heterozygosity, we focused on genes that showed significant differences in expression levels between Crebbp+/- and wild-type bone marrow stroma but no difference between Ep300+/- and wild-type. Bone marrow stroma was established from wild-type, Crebbp+/- and Ep300+/- mice that were 3-4 months old for RNA extraction and hybridization on Affymetrix microarrays. There are 4 biological replicates for each genotype used.

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CARM1 inhibition reduces histone acetyltransferase activity causing synthetic lethality in CREBBP/EP300 mutated lymphomas [RNA-seq_MEF]

Project description:Somatic mutations affecting CREBBP and EP300 are a hallmark of Diffuse Large B Cell Lymphoma (DLBCL). These mutations are frequently monoallelic, within the histone acetyltransferase (HAT) domain and usually mutually exclusive, suggesting that they might affect a common pathway and their residual WT expression is required for cell survival. Using in vitro and in vivo models, we found that inhibition of CARM1 activity (CARM1i) slows DLBCL growth and that the levels of sensitivity are positively correlated with the CREBBP/EP300 mutation load. Conversely, treatment of DLBCLs that do not have CREBBP/EP300 mutations with CARM1i and a CBP/p300 inhibitor revealed a strong synergistic effect. Our mechanistic data show that CARM1i further reduces the HAT activity of CBP genome wide and downregulates CBP target genes in DLBCL cells, resulting in a synthetic lethality that leverages the mutational status of CREBBP/EP300 as a biomarker for the use of small molecule inhibitors of CARM1 in DLBCL and other cancers.

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CARM1 inhibition reduces histone acetyltransferase activity causing synthetic lethality in CREBBP/EP300 mutated lymphomas [ChIP-seq]

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EP300/CREBBP acetyltransferase inhibition limits steroid receptor and FOXA1 signaling in prostate cancer cells (ChIP-seq)

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