Transcriptional dysregulation of BAHCC1 in melanoma [CUT&TAG_BAHCC1]
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ABSTRACT:
PROVIDER: PRJNA1034547 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional dysregulation of BAHCC1 in melanoma [CUT&Tag]
| PRJNA846108 | ENA
Project description:Transcriptional dysregulation of BAHCC1 in melanoma
| PRJNA846106 | ENA
Project description:Transcriptional addiction of cancer cells for Super-Enhancer (SE) associated genes has been proven through an extensive use of transcriptional inhibitors against specific co-activators toward which SE are esponentially dependent compared to canonical enhancers. However, each cancer type displays different sensitivity against this new class of drugs whose efficacy may vary according to their transcriptomic profile including the expression of enzymatic proteins able to confer intrinsic tolerance or resistance. Moreover, SE has been observed as well in healthy cells which point a realistic concern toward the specificity of transcriptional inhibitors and their side effects on healthy tissues. Therefore, we looked at SE-associated genes specific for cancer using melanoma as a model. Here, we identified BAHCC1 whose activity is higher in melanoma compare to other cancer types and normal tissues. BAHCC1 is a protein involved both in gene expression and genomic stability. To explore BAHCC1 role in gene expression, we performed functional studies in melanoma cells in basal conditions or upon BAHCC1 silencing. Strikingly, BAHCC1 regulates an E2F-dependent subset of genes together with SWI/SNF chromatin remodelling complex.
2023-11-04 | GSE246745 | GEO
Project description:Transcriptional addiction of cancer cells for Super-Enhancer (SE) associated genes has been proven through an extensive use of transcriptional inhibitors against specific co-activators toward which SE are esponentially dependent compared to canonical enhancers. However, each cancer type displays different sensitivity against this new class of drugs whose efficacy may vary according to their transcriptomic profile including the expression of enzymatic proteins able to confer intrinsic tolerance or resistance. Moreover, SE has been observed as well in healthy cells which point a realistic concern toward the specificity of transcriptional inhibitors and their side effects on healthy tissues. Therefore, we looked at SE-associated genes specific for cancer using melanoma as a model. Here, we identified BAHCC1 whose activity is higher in melanoma compare to other cancer types and normal tissues. BAHCC1 is a protein involved both in gene expression and genomic stability. To explore BAHCC1 role in gene expression, we performed functional studies in melanoma cells in basal conditions or upon BAHCC1 silencing. Strikingly, BAHCC1 regulates an E2F-dependent subset of genes together with SWI/SNF chromatin remodelling complex.
2022-06-03 | GSE205462 | GEO
Project description:Transcriptional dysregulation of BAHCC1 in melanoma [RNA-seq]
| PRJNA832708 | ENA
Project description:Transcriptional addiction of cancer cells for Super-Enhancer (SE) associated genes has been proven through an extensive use of transcriptional inhibitors against specific co-activators toward which SE are esponentially dependent compared to canonical enhancers. However, each cancer type displays different sensitivity against this new class of drugs whose efficacy may vary according to their transcriptomic profile including the expression of enzymatic proteins able to confer intrinsic tolerance or resistance. Moreover, SE has been observed as well in healthy cells which point a realistic concern toward the specificity of transcriptional inhibitors and their side effects on healthy tissues. Therefore, we looked at SE-associated genes specific for cancer using melanoma as a model. Here, we identified BAHCC1 whose activity is higher in melanoma compare to other cancer types and normal tissues. BAHCC1 is a protein involved both in gene expression and genomic stability. To explore BAHCC1 role in gene expression, we performed functional studies in melanoma cells in basal conditions or upon BAHCC1 silencing. Strikingly, BAHCC1 regulates an E2F-dependent subset of genes together with SWI/SNF chromatin remodelling complex.
2022-04-30 | GSE201702 | GEO
Project description:Trimethylation of histone H3 lysine 27 (H3K27me3) regulates gene repression, cell-fate determination and differentiation. We report that a conserved Bromo-Adjacent Homology (BAH) module of BAHCC1 (BAHCC1BAH) ‘recognizes’ H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and ChIP-seq-based analyses demonstrate that direct readout of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-lysine-binding ‘cage’ formed by BAHCC1BAH, mediating co-localization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is overexpressed in human acute leukemias and interacts with transcriptional co-repressors. In leukemia, depletion of BAHCC1, or disruption of the BAHCC1BAH:H3K27me3 interaction, causes de-repression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to suppression of oncogenesis. In mice, introduction of a germ-line mutation at Bahcc1 to disrupt its H3K27me3 engagement causes partial postnatal lethality, supporting a role in development. This study unveils a novel H3K27me3-directed transduction pathway in mammals that relies on a conserved BAH ‘reader’.
2020-11-05 | PXD021679 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-06-03 | GSE205463 | GEO
Project description:SALL4 builds a complex with histone deacetylases, and is thought to confer its effects epigenetically. Both loss of Sall4 and inhibition of HDAC2 leads to an invasiveness in human melanoma cells. To study co-occupancy of SALL4 and HDAC2, we employed CUT&RUN targeting SALL4 and HDAC2 in human melanoma cells (M010817).
2021-06-30 | E-MTAB-10163 | biostudies-arrayexpress
Project description:CUT&RUN LoV-U was performed against SMAD4 using two different antibodies in M170117 human melanoma cells under 4 conditions: Control (DMSO), TGFb, MEKi and TGFb + MEKi (Both).
2024-04-22 | E-MTAB-13951 | biostudies-arrayexpress