Effect of Ep300 silencing on gene expression of RAW264.7
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE247999 | GEO | 2024/01/31
REPOSITORIES: GEO
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Project description:Effect of Ep300 silencing on gene expression of RAW264.7
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Project description:Silencing of the somatic cell-type specific gene expression programs is a critical yet poorly understood step in nuclear reprogramming. To uncover chromatin-related pathways important for maintaining cell identity, we carried out a reprogramming screen using inhibitors of chromatin factors. Here we identify two independent acetyl-lysine competitive inhibitors targeting the bromodomains of coactivators EP300 and CBP as potent enhancers of reprogramming. EP300/CBP bromodomain inhibition is critical during early stages of reprogramming, significantly accelerates the emergence of iPSCs and, when combined with Dot1L inhibition, enables efficient derivation of human iPSCs with Oct4 and Sox2 alone. In contrast, complete inhibition of catalytic acetyl-transferase activity of EP300/CBP prevents reprogramming. Genome-wide expression analyses indicate that EP300/CBP bromodomain inhibition diminishes the expression of somatic-specific genes without affecting the induction of pluripotency regulators. Through expression analyses, we identify the master mesenchymal transcription factor PRRX1 as a functionally important target in reprogramming that is downregulated upon EP300/CBP bromodomain inhibition. Collectively, our data uncover a role for bromodomain-mediated interactions of EP300/CBP in sustaining cell type specific gene expression programs and maintaining somatic cell identity
2019-02-14 | GSE118218 | GEO
Project description:Silencing of the somatic cell-type specific gene expression programs is a critical yet poorly understood step in nuclear reprogramming. To uncover chromatin-related pathways important for maintaining cell identity, we carried out a reprogramming screen using inhibitors of chromatin factors. Here we identify two independent acetyl-lysine competitive inhibitors targeting the bromodomains of coactivators EP300 and CBP as potent enhancers of reprogramming. EP300/CBP bromodomain inhibition is critical during early stages of reprogramming, significantly accelerates the emergence of iPSCs and, when combined with Dot1L inhibition, enables efficient derivation of human iPSCs with Oct4 and Sox2 alone. In contrast, complete inhibition of catalytic acetyl-transferase activity of EP300/CBP prevents reprogramming. Genome-wide expression analyses indicate that EP300/CBP bromodomain inhibition diminishes the expression of somatic-specific genes without affecting the induction of pluripotency regulators. Through expression analyses, we identify the master mesenchymal transcription factor PRRX1 as a functionally important target in reprogramming that is downregulated upon EP300/CBP bromodomain inhibition. Collectively, our data uncover a role for bromodomain-mediated interactions of EP300/CBP in sustaining cell type specific gene expression programs and maintaining somatic cell identity
2019-02-14 | GSE124582 | GEO
Project description:Silencing of the somatic cell-type specific gene expression programs is a critical yet poorly understood step in nuclear reprogramming. To uncover chromatin-related pathways important for maintaining cell identity, we carried out a reprogramming screen using inhibitors of chromatin factors. Here we identify two independent acetyl-lysine competitive inhibitors targeting the bromodomains of coactivators EP300 and CBP as potent enhancers of reprogramming. EP300/CBP bromodomain inhibition is critical during early stages of reprogramming, significantly accelerates the emergence of iPSCs and, when combined with Dot1L inhibition, enables efficient derivation of human iPSCs with Oct4 and Sox2 alone. In contrast, complete inhibition of catalytic acetyl-transferase activity of EP300/CBP prevents reprogramming. Genome-wide expression analyses indicate that EP300/CBP bromodomain inhibition diminishes the expression of somatic-specific genes without affecting the induction of pluripotency regulators. Through expression analyses, we identify the master mesenchymal transcription factor PRRX1 as a functionally important target in reprogramming that is downregulated upon EP300/CBP bromodomain inhibition. Collectively, our data uncover a role for bromodomain-mediated interactions of EP300/CBP in sustaining cell type specific gene expression programs and maintaining somatic cell identity
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Project description:Transcriptional profiling of differential miRNA expression in mouse RAW264.7 preosteoclast cells comparing control untreated cells with RAW264.7 cells treated for 6 days. Treatment conditiones tested included 50ng/mL RANKL or indicated bone metastasis tumor cell conditioned media from 4T1, 4T1.2, TSU-PR1, and TSU-PR1-B2 cell lines.
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Project description:Gene expression is regulated by promoters and enhancers marked by histone H3-lysine-27 acetylation (H3K27ac), which is established by the paralogous histone acetyltransferases (HATs), EP300 and CBP. These enzymes display overlapping regulatory roles in untransformed cells, but less characterized roles in cancer cells. We demonstrate that the majority of high-risk pediatric neuroblastomas (NB) depend on EP300, whereas CBP has a limited role. EP300 controls enhancer acetylation by interacting with TFAP2?, a transcription factor member of the lineage-defining transcriptional core regulatory circuitry (CRC) in NB. To disrupt EP300, we developed a proteolysis-targeted-chimaera (PROTAC) compound termed ?JQAD1? that selectively targets EP300 for degradation. JQAD1 treatment causes loss of H3K27ac at CRC enhancers and neuroblastoma apoptosis, with limited toxicity to untransformed cells where CBP compensates. Comparing HAT inhibition and EP300-specific degradation, we identified a non-catalytic role for EP300 in promoting MYCN expression and repression of apoptosis.
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Project description:Gene expression is regulated by promoters and enhancers marked by histone H3-lysine-27 acetylation (H3K27ac), which is established by the paralogous histone acetyltransferases (HATs), EP300 and CBP. These enzymes display overlapping regulatory roles in untransformed cells, but less characterized roles in cancer cells. We demonstrate that the majority of high-risk pediatric neuroblastomas (NB) depend on EP300, whereas CBP has a limited role. EP300 controls enhancer acetylation by interacting with TFAP2?, a transcription factor member of the lineage-defining transcriptional core regulatory circuitry (CRC) in NB. To disrupt EP300, we developed a proteolysis-targeted-chimaera (PROTAC) compound termed ?JQAD1? that selectively targets EP300 for degradation. JQAD1 treatment causes loss of H3K27ac at CRC enhancers and neuroblastoma apoptosis, with limited toxicity to untransformed cells where CBP compensates. Comparing HAT inhibition and EP300-specific degradation, we identified a non-catalytic role for EP300 in promoting MYCN expression and repression of apoptosis.
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