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RNA-seq of murine small intestinal organoids treated with Ep300/Crebbp inhibitor I-CBP112 against untreated controls

ABSTRACT: RNA-seq of murine small intestinal organoids treated with Ep300/Crebbp inhibitor I-CBP112 against untreated controls

PROVIDER: PRJEB39194 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4314520.fastq.gz	Fastqsanger.gz
	ERR4314530.fastq.gz	Fastqsanger.gz
	ERR4314521.fastq.gz	Fastqsanger.gz
	ERR4314531.fastq.gz	Fastqsanger.gz
	ERR4314522.fastq.gz	Fastqsanger.gz

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RNA-seq of murine small intestinal organoids treated with Ep300/Crebbp inhibitor I-CBP112 against untreated controls

Project description:Murine small intestinal organoids were cultured in the presence or absence of 3µM inhibitor I-CBP112 (PubChem CID 90488984), which targets E1A Binding Protein P300 (Ep300) and Creb-binding protein (Crebbp, Cbp). Organoids were grown in culture media containing EGF, Noggin and R-spondin (ENR), media was changed after 48h, and organoids were harvested after 96h.

2020-12-16 | E-MTAB-9290 | biostudies-arrayexpress

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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Targeting CREBBP/EP300 bromodomains in cancer

Project description:Changes in gene expression caused by CREBBP/EP300 bromodomain inhibitors in a CML cell line

2018-06-12 | GSE110229 | GEO

H3K27Ac mapping in isogenic CREBBP-WT, CREBBP-KO and EP300-KO SUDHL4 cell lines

Project description:Inactivating mutations of the CREBBP acetyltransferase and, at lower frequencies, its paralogue EP300 are among the most common genetic alterations in diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL), the two most frequent B cell malignancies. Here we uncover unexpected distinct functions for CREBBP and EP300 in the germinal center (GC), i.e. the target structure for most human B cell lymphomas. We show that these proteins modulate non-overlapping transcriptional programs that are preferentially enriched in biological functions associated with the separate anatomic compartments of the GC. Consistently, deletion of CREBBP or EP300 have opposing effects on GC formation in vivo. Nonetheless, these proteins partially compensate for each other to maintain a minimal threshold of acetyltransferase activity and guarantee homeostatic control of the GC, which is completely abrogated by their combined loss. This synthetic lethal interaction is retained in DLBCL cells, identifying an Achille’s heel in CREBBP-mutant lymphomas that could be pharmacologically targeted by using a novel, selective small molecule inhibitor of the CREBBP/EP300 bromodomain. These data shed light on the unique roles of CREBBP and EP300 in the physiology and pathology of GC B cells, and provide a proof-of-principle for the development and testing of EP300 inhibition as a therapeutic strategy in these diseases.

2020-02-19 | GSE132365 | GEO

Targeting CREBBP/EP300 in cancer

Project description:Antiprolifereative effects of CREBBP/EP300 inhibitors were tested in human leukemia and lymphoma cell lines and the molecular mechanisms responsible for such effects were explored.

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

2011-03-01 | GSE24773 | GEO

Targeting CREBBP/EP300 bromodomains in cancer

Project description:Targeting CREBBP/EP300 bromodomains in cancer

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CREBBP/EP300 bromodomain inhibition affects the proliferation of AR positive breast cancer cell lines

Project description:Changes in gene expression caused by CREBBP/EP300 bromodomain inhibitors in breast cancer cell lines

2021-05-18 | GSE114937 | GEO

Bromodomain of CREBBP/EP300 cooperates with BNC2 to reprogram cell state in breast cancer

Project description:The plasticity of cancer cells influences their phenotypic and functional diversity. Understanding the mechanisms underlying cell state transitions, particularly the epithelial-mesenchymal transition (EMT) and its reverse process – mesenchymal-epithelial transition (MET), can provide insights into therapeutic strategies that control tumor progression and metastasis. Epigenetic reprogramming governs cellular plasticity. To survey epigenetic inhibitors capable of inducing MET, we employ a high-throughput small-molecule library screen coupled to a cell state reporter assay. We identify CREBBP/EP300 bromodomain inhibitor as a potent MET promoter, which specifically induces cell state transition in basal-like breast cancer but not luminal breast cancer. CREBBP/EP300 bromodomain inhibition leads to a gain in luminal characteristics and a reduction in stem-like properties. Strikingly, inhibiting the bromodomain of CREBBP/EP300, rather than its HAT domain, is more effective in promoting MET, decreasing tumorigenicity, and impeding metastasis. This underscores the finding that CREBBP/EP300 mediated cell state reprogramming is not attributed to changes in histone acetylation but likely converges on effector genes recognized by the bromodomain. Through transcriptomic and ChIP-Seq analyses, we find the zinc finger protein basonuclin-2 (BNC2) as a potential transcription factor involved in cell state regulation. Its interaction with CREBBP/EP300 bromodomain is essential for regulating super-enhancer-associated genes that maintain the mesenchymal cell state. These findings provide a new functional role for the bromodomain in epigenetic regulation and suggest strategies for therapeutic intervention in mesenchymal breast cancer.

2025-09-30 | GSE276326 | GEO

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.

2020-06-18 | GSE152666 | GEO

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