4T1 ATAC-seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE328671 | GEO | 2026/06/16
REPOSITORIES: GEO
Dataset's files
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| GSE328671_RAW.tar | Raw | |||
| filelist.txt | Txt |
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Project description:Mammalian SWI/SNF or BAF are multi-subunit complexes that regulate cell-type specific gene expression by modulating chromatin accessibility, in coordination with transcription factors and other chromatin regulators. PBRM1 is the complex defining subunit of PBAF class of SWI/SNF complexes. It is mutated in ~40% of clear cell renal cell carcinoma cases but also associated with cancer progression and therapy resistance, indicating context-dependent function. We have previously reported that loss of PBRM1 in normal epithelial cells results in a partial Epithelial-to-Mesenchymal Transition (EMT). In this study, we have utilized epigenomic and transcriptomic approaches to understand the mechanistic role of PBRM1 in EMT-regulated gene expression, and its relationship to genome-wide histone modifications.
2026-06-16 | GSE328672 | GEO
Project description:Mammalian SWI/SNF or BAF are multi-subunit complexes that regulate cell-type specific gene expression by modulating chromatin accessibility, in coordination with transcription factors and other chromatin regulators. PBRM1 is the complex defining subunit of PBAF class of SWI/SNF complexes. It is mutated in ~40% of clear cell renal cell carcinoma cases but also associated with cancer progression and therapy resistance, indicating context-dependent function. We have previously reported that loss of PBRM1 in normal epithelial cells results in a partial Epithelial-to-Mesenchymal Transition (EMT). In this study, we have utilized epigenomic and transcriptomic approaches to understand the mechanistic role of PBRM1 in EMT-regulated gene expression, and its relationship to genome-wide histone modifications.
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Project description:Mammalian SWI/SNF or BAF are multi-subunit complexes that regulate cell-type specific gene expression by modulating chromatin accessibility, in coordination with transcription factors and other chromatin regulators. PBRM1 is the complex defining subunit of PBAF class of SWI/SNF complexes. It is mutated in ~40% of clear cell renal cell carcinoma cases but also associated with cancer progression and therapy resistance, indicating context-dependent function. We have previously reported that loss of PBRM1 in normal epithelial cells results in a partial Epithelial-to-Mesenchymal Transition (EMT). In this study, we have utilized epigenomic and transcriptomic approaches to understand the mechanistic role of PBRM1 in EMT-regulated gene expression, and its relationship to genome-wide histone modifications.
2026-06-16 | GSE310185 | GEO
Project description:Mammalian SWI/SNF or BAF are multi-subunit complexes that regulate cell-type specific gene expression by modulating chromatin accessibility, in coordination with transcription factors and other chromatin regulators. PBRM1 is the complex defining subunit of PBAF class of SWI/SNF complexes. It is mutated in ~40% of clear cell renal cell carcinoma cases but also associated with cancer progression and therapy resistance, indicating context-dependent function. We have previously reported that loss of PBRM1 in normal epithelial cells results in a partial Epithelial-to-Mesenchymal Transition (EMT). In this study, we have utilized epigenomic and transcriptomic approaches to understand the mechanistic role of PBRM1 in EMT-regulated gene expression, and its relationship to genome-wide histone modifications.
2026-06-16 | GSE298752 | GEO
Project description:Mammalian SWI/SNF or BAF are multi-subunit complexes that regulate cell-type specific gene expression by modulating chromatin accessibility, in coordination with transcription factors and other chromatin regulators. PBRM1 is the complex defining subunit of PBAF class of SWI/SNF complexes. It is mutated in ~40% of clear cell renal cell carcinoma cases but also associated with cancer progression and therapy resistance, indicating context-dependent function. We have previously reported that loss of PBRM1 in normal epithelial cells results in a partial Epithelial-to-Mesenchymal Transition (EMT). In this study, we have utilized epigenomic and transcriptomic approaches to understand the mechanistic role of PBRM1 in EMT-regulated gene expression, and its relationship to genome-wide histone modifications.
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Project description:PBRM1 is lost in 40% of clear cell renal cell carcinomas (ccRCC) and the combined loss of VHL and PBRM1 drives ccRCC tumorigenesis. PBRM1 is an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler and despite its well-established role as a tumor suppressor, we have limited understanding of how PBRM1 regulates the chromatin. Now we report that PBRM1 binds to promoter-proxy regions with footprints at +1 to + 3 nucleosomes. PBRM1-deficient PBAF complexes lose BRD7 but retain ARID2, while tethered to SMARCA4. The lack of PBRM1-BRD7 module compromises the targeting specificity of the PBAF complexes, causes their genomic redistribution and impairs the repressive ability of PBAF complexes. Subsequently, PBRM1-deficient PBAF complexes prime the chromatin at de novo sites for transcriptional activation of pro-survival genes involved in hypoxia and cholesterol synthesis. Therefore, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-survival genes by residual PBRM1-deficient SWI/SNF complexes.
2021-07-24 | PXD020553 | JPOST Repository
Project description:PBRM1 is lost in 40% of clear cell renal cell carcinomas (ccRCC) and the combined loss of VHL and PBRM1 drives ccRCC tumorigenesis. PBRM1 is an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler and despite its well-established role as a tumor suppressor, we have limited understanding of how PBRM1 regulates the chromatin. Now we report that PBRM1 binds to promoter-proxy regions with footprints at +1 to + 3 nucleosomes. PBRM1-deficient PBAF complexes lose BRD7 but retain ARID2, while tethered to SMARCA4. The lack of PBRM1-BRD7 module compromises the targeting specificity of the PBAF complexes, causes their genomic redistribution and impairs the repressive ability of PBAF complexes. Subsequently, PBRM1-deficient PBAF complexes prime the chromatin at de novo sites for transcriptional activation of pro-survival genes involved in hypoxia and cholesterol synthesis. Therefore, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-survival genes by residual PBRM1-deficient SWI/SNF complexes.
2021-07-24 | PXD020554 | JPOST Repository
Project description:Epigenetic dysregulation is a major cancer hallmark. Notably, deleterious mutations in genes encoding subunits of SWI/SNF (SWItch Sucrose Non-Fermentable), a major chromatin remodeling complex, occur in approximately 20% of human solid tumors. SWI/SNF mutations have been linked to poor patient outcome and no targeted therapy is currently available to treat patients with SWI/SNF-deficient tumors. SWI/SNF is a modular complex composed of 12-15 subunits encoded by 29 genes, which exist in three forms: canonical BRG1/BRM associated factor (cBAF), polybromo-associated BAF (PBAF) and non-canonical (ncBAF/GBAF), which have variable compositions, targets and effects on chromatin remodeling. Each complex includes core subunits (SMARCC1, SMARCC2, and SMARCD1-3) and one of the two mutually exclusive ATPase subunits (SMARCA2 or SMARCA4). Multiple variant subunits then define each complex’s specificity: ARID1A/B and DPF1-3 for cBAF; ARID2, PBRM1, BRD7 and PHF10 for PBAF; GLTSCR1/1L and BRD9 for ncBAF2. SWI/SNF orchestrates multiple cellular functions, such as transcription regulation, differentiation, proliferation, DNA repair, and immunogenicity. Still, subunit-specific oncogenic mechanisms or targetable dependencies remain poorly understood. To identify intracellular alterations and genetic vulnerabilities induced by SWI/SNF defects at the complex or subunit level, we molecularly and functionally profiled an isogenic panel of HAP1 cell lines knockout (KO) for chromatin remodeling encoding genes, including seven SWI/SNF subunits mutants (SMARCB1-, SMARCA4-, SMARCA2-, ARID1A-, ARID1B-, ARID2- and PBRM1-KO), and six non-SWI/SNF mutants (CREBBP-, BAP1-, EED-, KMT2C-, KMT2D- and SETD2-KO). 70-80% confluent cells were harvested, and total RNA was extracted using Rneasy Mini Kit (Qiagen, 74104) with DNAse treatment, according to the manufacturer’s instructions. Every RNA sample was quantified with a Qubit Fluorometer and evaluated for quality controls using Agilent 2100 Bioanalyzer Instrument (RRID:SCR_018043). After RNA Integrity Number (RIN) quality control, cDNA libraries were generated using the NEBNext Ultra II RNA Library Prep Kit (NEB #E7775) on Bravo Automated Liquid Handling Platform (RRID:SCR_026137). Subsequent indexed RNA sequencing of cDNA libraries with paired-end reads was performed according to the standard Illumina protocol using Illumina NovaSeq 6000 S2 Sequencing System (RRID:SCR_016387), with a target of 100Gb per sample.
2025-10-20 | E-MTAB-15673 | biostudies-arrayexpress
Project description:The composition of chromatin remodeling complexes dictates how these enzymes control transcriptional programs and cellular identity. Here, we investigate the composition of SWI/SNF complexes in embryonic stem cells (ESCs). In contrast to differentiated cells, ESCs have a biased incorporation of certain paralogous SWI/SNF subunits, with low levels of Brm, BAF170 and ARID1B. Upon differentiation, the expression of these subunits increases, resulting in a higher diversity of compositionally distinct SWI/SNF enzymes. We also identify Brd7 as a novel component of the PBAF complex in both ESCs and differentiated cells. Using shRNA-mediated depletion of Brg1, we show that SWI/SNF can function as both a repressor and an activator in pluripotent cells, regulating expression of developmental modifiers and signaling components such as Nodal, ADAMTS1, Bmi-1, CRABP1 and TRH. Knock-down studies of PBAF-specific Brd7 and of a signature subunit within the BAF complex, ARID1A, show that these two sub-complexes affect SWI/SNF target genes differentially, in some cases even antagonistically. This may be due to their different biochemical properties. Finally, we examine the role of SWI/SNF in regulating its target genes during differentiation. We find that SWI/SNF affects recruitment of components of the pre-initiation complex in a promoter-specific manner, to modulate transcription positively or negatively. Taken together, our results provide insight into the function of compositionally diverse SWI/SNF enzymes that underlie their inherent gene-specific mode of action. R1 ESCs were infected in duplicates with shRNA targeting Brg1 or GLUT4 (as a control). Knockdown of Brg1 mRNA affected Brg1 protein levels efficiently. RNA was isolated 67 hours post-infection and analyzed using microarrays.
2010-03-04 | E-GEOD-7791 | biostudies-arrayexpress
Project description:PBRM1 is an accessory subunit of the PBAF subclass of the SWI/SNF chromatin remodeler. The inactivation of PBRM1 is the second most frequent mutational event in kidney tumorigenesis. Here we show that in VHL-deficient ccRCC tumors, PBRM1 loss results in an altered PBAF complex that retains the association between SMARCA4 and ARID2 but disengages BRD7 from SMARCA4. The PBRM1-deficient PBAF complexes redistribute from promoter proxy regions to distal enhancer regions. The ATPase function of SMARCA4 enhances the recruitment of nuclear factor RELA to aberrant sites and promotes NF-κB activity. Proteasome inhibitor bortezomib reverses NF-κB activation by reducing RELA binding at regions bound by PBRM1-deficient PBAF and delays PBRM1-deficient tumor growth. In conclusion, PBRM1 safeguards the chromatin by repressing aberrant liberation of pro-tumorigenic NF-κB target genes by residual PBRM1-deficient PBAF complexes.
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