PBRM1 RNA-seq
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE269428 | GEO | 2026/06/16
REPOSITORIES: GEO
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| GSE269428_counts_set1.xlsx | Xlsx | |||
| GSE269428_counts_set2.xlsx | Xlsx | |||
| GSE269428_counts_set3.xlsx | Xlsx |
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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.
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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.
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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.
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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.
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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.
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