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Gene expression regulation in MCF7 cells by H3B-6545, H3B-9709, Fulvestrant and Tamoxifen

ABSTRACT: In the cellular setting, both H3B-6545 and H3B-9709 were confirmed to be non-degraders and had nearly identical impact on global gene expression changes

ORGANISM(S): Homo sapiens

PROVIDER: GSE178303 | GEO | 2022/03/15

REPOSITORIES: GEO

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Genome-wide ERa DNA-binding in MCF7 cells revealed by ChIP-seq

Project description:In the cellular setting, both H3B-6545 and H3B-9709 were confirmed to be non-degraders and had similar global DNA-binding patterns.

2022-03-15 | GSE178368 | GEO

Gene expression regulation in MCF7 cells by H3B-6545, H3B-9709, Fulvestrant and Tamoxifen

Project description:Gene expression regulation in MCF7 cells by H3B-6545, H3B-9709, Fulvestrant and Tamoxifen

| PRJNA738454 | ENA

RNA-seq and ChIP-seq in MCF7 cells treated with H3B-6545, H3B-9709, Fulvestrant and Tamoxifen

Project description:RNA-seq and ChIP-seq in MCF7 cells treated with H3B-6545, H3B-9709, Fulvestrant and Tamoxifen

| PRJNA738710 | ENA

RNA-seq and ChIP-seq in MCF7 cells treated with H3B-6545, H3B-9709, Fulvestrant and Tamoxifen

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-15 | GSE178373 | GEO

Transcriptional profiling of Ishikawa cells treated with H3B-5942, E2, or standard of care compounds

Project description:The objective of this experiment was to determine the affect of H3B-5942 treatment on global gene expression in an estrogen-deprived setting (agonist mode) and to compare to treatment with a saturated analog of H3B-5942, GDC-0810, and standard of care agents tamoxifen and fulvestrant.

2018-06-12 | GSE115608 | GEO

ChIP-Seq analysis of estrogen deprived MCF7 cells treated with H3B-5942 and standards of care compounds

Project description:The goal of this experiment was to interrogate the potential transcriptional impact of H3B-5942 by investigating its influence on genome-wide DNA-binding modes of ERa in MCF7 cells using chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-Seq). Affects of H3B-5942 on chromatin recruitment were compared to results from treatment with E2, 4-OHT, and fulvestrant.

2018-06-12 | GSE115607 | GEO

H3B-8800, a novel oral splicing modulator, induces lethality in spliceosome mutant cancers [K562]

Project description:Genomic analyses of cancer have identified recurrent point mutations in the RNA splicing factors SF3B1, U2AF1, and SRSF2 that confer an alteration of function. Although cells bearing these mutations are preferentially dependent on wild-type (WT) spliceosome function, clinical means to therapeutically target the spliceosome do not currently exist. Here, we describe an orally available modulator of the SF3b complex, H3B-8800, which potently and selectively kills spliceosome-mutant epithelial and hematologic malignancies. The effects of H3B-8800 are entirely selective for the Sf3b complex, as evidenced by the identification of drug-resistant cells bearing mutations in Sf3b components. Although H3B-8800 modulates RNA splicing mediated by WT or cancer-associated SF3B1 mutants, its preferential effects on spliceosome-mutant cells is due to preferred retention of short, GC-rich introns, which are enriched in genes encoding a substantial number of spliceosome components. These data demonstrate the therapeutic potential of splicing modulation in spliceosome-mutant cancers.

2017-12-20 | GSE94528 | GEO

Chronic Lymphocytic Leukemia MEC1 SF3B1 K700E and Wild Type Cell Lines' RNA-seq after Treatment with H3B-8800 Splicing Modulator.

Project description:To study the impact of SF3B1 mutations on alternative splicing and the effect of H3B-8800 splicing modulator in wild type and SF3B1-mutant chronic lymphocytic leukemia cells, we established SF3B1 K700E MEC1 CLL isogenic cell line and carried out RNA deep sequencing in SF3B1 wild type and K700E MEC1 cell lines upon H3B-8800 treatment.

2023-08-08 | GSE190087 | GEO

H3B-8800, a novel oral splicing modulator, induces lethality in spliceosome mutant cancers [Nalm-6]

2017-12-20 | GSE94999 | GEO

RNA-seq analysis of combination effect of H3B-6527 and Lenvatinib treatment in the Hep3B in vivo model

Project description:To investigate the underlying mechanism of the enhanced combination effect of H3B-6527 and Lenvatinib, we conducted RNA-seq analysis of Hep3B cell line xenograft tumors following treatment of tumor bearing mice with one dose of H3B-6527 or Lenvatinib as single agents or in combination. Principal component analysis and hierarchical clustering of differentially expressed genes (differentially expressed genes with adjusted p value < 0.05) showed two largely separated groups in which vehicle and Lenvatinib samples are close to each other whereas the H3B-6527 and the combination samples show similar pattern (Fig. 4A and 4B), suggesting Lenvatinib at 10mg/kg does not drastically alter transcriptional profiles of tumor cells. We then performed pathway enrichment analysis of differentially expressed genes, which showed bile acid metabolism as the top upregulated pathway in H3B-6527 single-agent group, a well-known selective effect to the FGFR4 signaling pathway (Fig. 4C). E2F targets and MYC targets scored as the top downregulated pathways; an effect that is common among many receptor tyrosine kinases including FGFR4. Combination of H3B-6527 and Lenvatinib showed significant upregulation of hypoxia and glycolysis pathways, consistent with anti-angiogenic effect resulting in lack of oxygen and nutrients in tumor microenvironment (Fig. 4C). Moreover, the combination groups showed stronger effects on E2F targets as compared with the single agent groups, and explains the increased antitumor activity observed in efficacy experiments (Fig. 4D). In summary, the RNAseq analysis provided direct mechanistic evidence for the combined anti-angiogenic and anti-tumorigenic effects resulting in enhanced efficacy.

2022-07-13 | GSE198845 | GEO

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