BRD7 overexpression cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA275626 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1805900.fastq.gz | Fastqsanger.gz | |||
| SRR1805899.fastq.gz | Fastqsanger.gz | |||
| SRR1810500.fastq.gz | Fastqsanger.gz | |||
| SRR1810499.fastq.gz | Fastqsanger.gz |
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Project description:Oncogene-induced senescence (OIS) is a p53-dependent defence mechanism against uncontrolled proliferation. Consequently, many human tumours harbour p53 mutations while others show a dysfunctional p53 pathway, frequently by unknown mechanisms. We identified BRD7, a bromodomain-containing protein whose inhibition allows full neoplastic transformation in the presence of wild-type p53. Intriguingly, in human breast tumours harbouring wild-type, but not mutant p53, the BRD7 gene locus was frequently deleted and low BRD7 expression was found in a subgroup of tumours. Functionally, BRD7 is required for efficient p53-mediated transcription of a subset of target genes. BRD7 interacts with p53 and p300, and is recruited to target gene promoters, affecting histone acetylation, p53 acetylation, and promoter activity. Thus, BRD7 suppresses tumourigenicity by serving as a p53 cofactor required for efficient induction of p53-dependent OIS. We recorded mRNA expression profiles of BJ primary fibroblasts expressing the oncogene RasV12 and either control vector, one of two BRD7 knockdown vectors, or p53 knockdown vector. In addition, we profiled genome-wide protein DNA interactions for p53 and BRD7 using ChIP-Seq. p53- and BRD7-binding sites were recorded in RasV12-expressing BJ cells; as a control we used knockdown of the gene of interest (BRD7 or p53).
2010-03-14 | E-GEOD-20076 | biostudies-arrayexpress
Project description:We applied Chromatin immunoprecipation and massively parallel DNA sequencing technique, ChIP-seqencing, to identify the binding sites of Brd7 protein in human cells. ChIP-seq was applied to HEK293 cell line in control and BRD7 overexpressed cells.
2018-02-12 | GSE65974 | GEO
Project description:We applied digital gene expression profiling to HEK293 cell line in control and BRD7 overexpressed cells, to investigate the globle differently gene expression.
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Project description:Transcriptional profiling of human BJ fibroblasts comparing control FF shRNA expressing cells vs. BRD7 shRNA expressing cells under two conditions, either untreated or treated with 8uM nutln-3a for 8 hours. This experiment was done using two independent shRNAs targeting BRD7. Nutlin-3a was used to stabilize p53 and induce its transcriptional activity. Two-condition experiment, FF shRNA cells vs. BRD7 shRNAs cells in two experimental conditions, either untreated or treated with nutlin-3a.
2010-07-01 | E-GEOD-22607 | biostudies-arrayexpress
Project description:Metastasis is a major cause of mortality in cancer and is likely influenced by epigenetic and gene regulatory factors. Using an in vivo screen, we demonstrated that several subunits of the polybromo-associated BAF (PBAF) complex, particularly BRD7, were required for breast cancer metastatic dormancy in lung. BRD7 loss induced metastatic outgrowth, along with modifications in epigenomic landscapes and upregulated oncogenic signaling. Breast cancer cells harboring BRD7 loss also reprogrammed the surrounding immune microenvironment, downregulating MHC-1 expression and promoting a pro-metastatic cytokine profile. Flow cytometric and single-cell analyses revealed increased levels of pro-tumorigenic neutrophils, CD8+ exhausted T cells, and CD4+ stress response T cells in lungs harboring BRD7-deficient metastases. Finally, attenuating this immunosuppressive milieu by neutrophil depletion, neutrophil extracellular trap (NET) inhibition, or immune checkpoint therapy abrogated metastatic outgrowth. These findings, for the first time, implicate BRD7 and PBAF in metastasis, pointing to targetable underlying mechanisms involving specific immune cell compartments.
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Project description:Metastasis is a major cause of mortality in cancer and is likely influenced by epigenetic and gene regulatory factors. Using an in vivo screen, we demonstrated that several subunits of the polybromo-associated BAF (PBAF) complex, particularly BRD7, were required for breast cancer metastatic dormancy in lung. BRD7 loss induced metastatic outgrowth, along with modifications in epigenomic landscapes and upregulated oncogenic signaling. Breast cancer cells harboring BRD7 loss also reprogrammed the surrounding immune microenvironment, downregulating MHC-1 expression and promoting a pro-metastatic cytokine profile. Flow cytometric and single-cell analyses revealed increased levels of pro-tumorigenic neutrophils, CD8+ exhausted T cells, and CD4+ stress response T cells in lungs harboring BRD7-deficient metastases. Finally, attenuating this immunosuppressive milieu by neutrophil depletion, neutrophil extracellular trap (NET) inhibition, or immune checkpoint therapy abrogated metastatic outgrowth. These findings, for the first time, implicate BRD7 and PBAF in metastasis, pointing to targetable underlying mechanisms involving specific immune cell compartments.
2024-12-06 | GSE262165 | GEO
Project description:Transcriptional profiling of human BJ fibroblasts comparing control FF shRNA expressing cells vs. BRD7 shRNA expressing cells under two conditions, either untreated or treated with 8uM nutln-3a for 8 hours. This experiment was done using two independent shRNAs targeting BRD7. Nutlin-3a was used to stabilize p53 and induce its transcriptional activity.
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Project description:Metastasis is a major cause of mortality in cancer and is likely influenced by epigenetic and gene regulatory factors. Using an in vivo screen, we demonstrated that several subunits of the polybromo-associated BAF (PBAF) complex, particularly BRD7, were required for breast cancer metastatic dormancy in lung. BRD7 loss induced metastatic outgrowth, along with modifications in epigenomic landscapes and upregulated oncogenic signaling. Breast cancer cells harboring BRD7 loss also reprogrammed the surrounding immune microenvironment, downregulating MHC-1 expression and promoting a pro-metastatic cytokine profile. Flow cytometric and single-cell analyses revealed increased levels of pro-tumorigenic neutrophils, CD8+ exhausted T cells, and CD4+ stress response T cells in lungs harboring BRD7-deficient metastases. Finally, attenuating this immunosuppressive milieu by neutrophil depletion, neutrophil extracellular trap (NET) inhibition, or immune checkpoint therapy abrogated metastatic outgrowth. These findings, for the first time, implicate BRD7 and PBAF in metastasis, pointing to targetable underlying mechanisms involving specific immune cell compartments.
2024-12-06 | GSE267197 | GEO
Project description:Metastasis is a major cause of mortality in cancer and is likely influenced by epigenetic and gene regulatory factors. Using an in vivo screen, we demonstrated that several subunits of the polybromo-associated BAF (PBAF) complex, particularly BRD7, were required for breast cancer metastatic dormancy in lung. BRD7 loss induced metastatic outgrowth, along with modifications in epigenomic landscapes and upregulated oncogenic signaling. Breast cancer cells harboring BRD7 loss also reprogrammed the surrounding immune microenvironment, downregulating MHC-1 expression and promoting a pro-metastatic cytokine profile. Flow cytometric and single-cell analyses revealed increased levels of pro-tumorigenic neutrophils, CD8+ exhausted T cells, and CD4+ stress response T cells in lungs harboring BRD7-deficient metastases. Finally, attenuating this immunosuppressive milieu by neutrophil depletion, neutrophil extracellular trap (NET) inhibition, or immune checkpoint therapy abrogated metastatic outgrowth. These findings, for the first time, implicate BRD7 and PBAF in metastasis, pointing to targetable underlying mechanisms involving specific immune cell compartments.
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Project description:The Epstein-Barr virus (EBV) switches between latent and lytic phases in hosts that are important in developing related diseases. However, the underlying mechanism of how the viral latent-lytic switch is controlled and how EBV itself mediates this regulation remains largely unknown. This study identified the upregulated histone acetyl reader bromodomain-containing protein 7 (BRD7) during EBV latent infection. Based on the ChIP-sequencing of endogenous BRD7 in Burkitt lymphoma cells, we found that EBV drove BRD7 to regulate cellular and viral genomic loci, including the transcriptional activation of c-Myc, a recently reported regulator of EBV latency. Additionally, EBV-mediated BRD7 signals enriched around the FUSE site in chromosome 8, and the enhancer LOC108348026 in the lgH locus, which might activate the c-Myc alleles. Mechanically, EBV-encoded nuclear antigen 1 (EBNA1) bound and recruited BRD7 to colocalize at promotor regions of the related genes, thus serving as cofactors for the maintenance of viral latency. Moreover, the disruption of BRD7 decreased the c-Myc expression, induced the BZLF1 expression, and reactivated the lytic cycle. Our findings reveal the unique role of BRD7 hijacked by EBV in maintaining the viral latency state via chromatin remodeling. The study paved the way for understanding the new molecular mechanism of EBV-induced chromatin remodeling and latent-lytic switch regulation, providing novel therapeutic candidate targets for EBV persistent infection. With establishing persistent infection in most human hosts, EBV is usually at a latent infection state. How the viral latency is maintained in cells remains largely unknown. c-Myc was recently reported to act as a controller of the lytic switch, while whether and how EBV regulates it remains to be explored. Here, we identified that BRD7 is involved in controlling EBV latency. We found that EBV-mediated BRD7 was enriched in both the normal promoter regions and the translocation alleles of c-Myc, and the disruption of BRD7 decreased c-Myc expression to reactivate the lytic cycle. We also demonstrated that EBV-encoded EBNA1 bound to and regulated BRD7. Therefore, we reveal a novel mechanism by which EBV can regulate its infection state by hijacking host BRD7 to target c-Myc. Our findings will help future therapeutic intervention strategies of EBV infection and pathogenesis.
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