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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE114937 | GEO | 2021/05/18

REPOSITORIES: GEO

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

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

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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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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

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Transcriptional profiling of murine germinal center (GC) B cells from GC-specific conditional Crebbp and Ep300 knock-out mice

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MYC-mediated ribosomal gene expression sensitizes enzalutamide-resistant cells to EP300/CREBBP inhibitors

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