The effect of knockout Brd7 on 4T07-TGL cells under in vitro condition
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PROVIDER: PRJNA1090500 | ENA |
REPOSITORIES: ENA
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Project description:the effect of knockout Brd7 on 4T07-TGL cells under in vitro condition
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Project description:The effect of knockout Brd7 on 4T07-TGL cells under in vitro condition [RNA-seq]
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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: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 | GSE260497 | 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: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: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.
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Project description:To determine the molecular mechanisms by which Six2 regulates metastatic colonization, we performed RNA-seq analysis on murine triple-negative 4T07 Control (4T07-CTL) and Six2 overexpressing (4T07-Six2) cells. Using both targeted and unbiased gene signature analyses, we found that Six2 differentially regulates gene signatures associated with stemness. Additionally, we confirmed that in several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes (identified as among the highest upregulated genes in response to Six2 overexpression) associated with embryonic stem cell programs. When combined with our in vitro and in vivo stemness-associated phenotypic assays, these data suggest that Six2 may play a similar role in mediating stemness characteristics during tumor progression as it does during development, and that this role may allow it to mediate late-stage metastasis by enhancing the ability of cells to self-renew and survive at secondary sites.
2020-01-30 | GSE123489 | GEO
Project description:RNA-seq Analysis in 4T07 Control (4T07-CTL) and Six2 Overexpression (4T07-Six2) cells
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