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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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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

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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.

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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

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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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