Transcriptomic analysis of Bptf wild-type and Bptf heterozygous lymphomas arising from Em-Myc tumors
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PROVIDER: PRJNA594301 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: Evaluation of the impact of a reduction in Bptf levels on the nature of lymphomas arising from Em-Myc mice. Results: Bptf heterozygous tumors show reduced activity of the E2F and c-MYC pathways, together with increased activity of the NF-kB pathway.
2019-12-10 | GSE141647 | GEO
Project description:Ezh2 encodes for the catalyc unit of the PRC2 complex. RNAi-mediated suppressing of Ezh2 by two independent shRNAs promotes Em-myc lymphomagenesis in vivo. Microarray were used to explore the trascriptional changes driven by suppression of Ezh2 in Em-myc cells and to identify which programs contribute to promotion of lymphoma formation.
2015-02-01 | GSE64537 | GEO
Project description:Ezh2 encodes for the catalyc unit of the PRC2 complex. RNAi-mediated suppressing of Ezh2 by two independent shRNAs promotes Em-myc lymphomagenesis in vivo. Microarray were used to explore the trascriptional changes driven by suppression of Ezh2 in Em-myc cells and to identify which programs contribute to promotion of lymphoma formation. RNA was extracted from purified primary lymphoma cells for each shRNAs targeting Ezh2 and from two independent preparations of premalignant Em-myc cells. Mouse Genome 1.0 ST arrays were processed according to the manifacturer`s instructions.
2015-02-01 | E-GEOD-64537 | biostudies-arrayexpress
Project description:We investigated brain tissue from N471D WASH complex subunit strumpellin knock-in mice as a genetic model for hereditary spastic paraplegia type 8. While WASHC5-related protein interaction partners and complexes showed no change in abundancies, the proteomic analysis depicted consistent upregulation of BPTF and downregulation of KLHL11 in heterozygous and homozygous knock-in mice. This finding suggests mechanistic links for hereditary spastic paraplegia type 8 through the roles of BPTF and KLHL11 in neurodegeneration and protein quality control, respectively.
2021-07-26 | PXD025315 | Pride
Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)
2016-01-19 | E-GEOD-65545 | biostudies-arrayexpress
Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)
2016-01-19 | E-GEOD-65544 | biostudies-arrayexpress
Project description:Palb2 interacts with BRCA1 and BRCA2 in supercomplexes involved in DNA repair via homologous recombination. Heterozygous germline mutations in PALB2 confer a moderate risk of breast cancer while biallelic PALB2 mutations are linked to a severe form of Fanconi anaemia characterized by early childhood solid tumours and severe chromosomal instability. In contrast to BRCA1- or BRCA2-associated cancers, breast tumours in heterozygous PALB2 mutation carriers do not show loss of the wild type allele, suggesting PALB2 might be haploinsufficient for tumour suppression. To study the role of PALB2 in development and tumourigenesis, we have generated Palb2GT mouse mutants using a gene trap approach. Whereas Palb2GT/GT homozygous mutant embryos died at mid-gestation due to massive apoptosis, Palb2GT/+ heterozygous mice were viable and did not show any obvious abnormalities. Deletion of p53 alleviated the phenotype of Palb2GT/GT embryos, but did not rescue embryonic lethality. In addition, loss of p53 did not significantly collaborate with Palb2 heterozygosity in tumourigenesis in heterozygous or homozygous p53 knockout mice. Tumours arising in Palb2GT/+;p53+/– or Palb2GT/+;p53–/– compound mutant mice retained the wild type Palb2 allele and did not display increased genomic instability. Comparison of 15 Palb2GT/+;p53-/- and 11 Palb2+/+;p53-/- lymphomas. Spleen/liver DNA of the same animal was used as reference material.
2011-01-21 | E-GEOD-26723 | biostudies-arrayexpress
Project description:In mouse models, the bromodomain PHD finger transcription factor (BPTF) chromatin remodeling subunit in tumor cells suppresses natural killer (NK) cell antitumor activity. In vitro, BPTF suppresses NK cell cytolytic activity to mouse and human cancer cell lines, demonstrating a conserved function.
2017-04-28 | GSE85756 | GEO
Project description:JAK1/2 inhibitor therapy-associated lymphomas in myelofibrosis arising from a pre-existing B-cell clone
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Project description:To understand how BPTF conferred resistance to Erlotinib in GC cells, we performed transcriptome profiling (RNA-seq) in MGC803/BPTF-KO and MGC803/BPTF-NC cells.
2023-12-13 | GSE200182 | GEO