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RDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq UTF]

ABSTRACT: Analysis of Upstream Binding Transcription Factor (UBTF) binding patterns by ChIP-seq in mouse wildtype, premalignant and malignant Eμ-Myc cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE123324 | GEO | 2019/02/06

REPOSITORIES: GEO

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rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq]

Project description:Analysis of PolI and H3K27me3 binding patterns by ChIP-seq in mouse wildtype, premalignant and malignant Eμ-Myc cells.

2019-08-01 | GSE70225 | GEO

rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [4C-seq]

Project description:Long-range interactions of ribososomal DNA (rDNA) identified by 4C-seq in mouse wildtype, premalignant and malignant Eμ-Myc cells and tissue culture adapated Eμ-Myc-shUbtf and Eμ-Myc-LMP (empty vector) cells.

2019-02-06 | GSE70221 | GEO

rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [RNA-seq]

Project description:Analysis of gene expression by RNA-seq in mouse wildtype, premalignant and malignant Eμ-Myc cells.

2019-02-06 | GSE70224 | GEO

rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq UTF]

Project description:rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq UTF]

| PRJNA508322 | ENA

rDNA chromatin interactions in the MYC-driven Eµ-Myc transgenic mouse model of B-cell lymphoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-06 | GSE70226 | GEO

Effect of NEK2 deficiency on gene expression of CD19-selected spleen B cells of Eμ-myc mouse model

Project description:NEK2 overexpression in the B cell lineage affects B cell development. To determine whether deficiency of NEK2 inhibits B cell malignancies, we crossed Nek2 knockout mice with Eμ-myc transgenic mice, a well-established Myc-driven preclinical model for B cell malignancies. Three genotyping offsprings were obtained: Eμ-myc/Nek2+/+ (NEK2 wild type), Eμ-myc/Nek2+/- (NEK2 heterozygotes), and Eμ-myc/Nek2-/- (NEK2 homozygotes). Bulk RNA-seq was performed on CD19-selected spleen B cells to view the transcriptome differences.

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Gene expression and polysome profiling data of Eμ-Myc B-lymphoma cells

Project description:Gene expression and polysome profiling data of Eμ-Myc B-lymphoma cells

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IBTK contributes to B-cell lymphomagenesis in Eμ-myc transgenic mice conferring resistance to apoptosis.

Project description:Increasing evidence supports the involvement of IBTK in cell survival and tumor growth. Previously, we have shown that IBTK RNA interference affects the wide genome expression and RNA splicing in cell-type specific manner. Further, the expression of IBTK gene progressively increases from indolent to aggressive stage of chronic lymphocytic leukemia and decreases in disease remission after therapy. However, the role of IBTK in tumorigenesis has not been elucidated. Here, we report that loss of the murine Ibtk gene raises survival and delays tumor onset in Eμ-myc transgenic mice, a preclinical model of Myc-driven lymphoma. In particular, we found that the number of pre-cancerous B cells of bone marrow and spleen is reduced in Ibtk-/-Eμ-myc mice owing to impaired viability and increased apoptosis, as measured by Annexin V binding, Caspase 3/7 cleavage assays and cell cycle profile analysis. Instead, the proliferation rate of pre-cancerous B cells is unaffected by the loss of Ibtk. We observed a direct correlation between Ibtk and myc expression and demonstrated a Myc-dependent regulation of Ibtk expression in murine B cells, human hematopoietic and nonhematopoietic cell lines by analysis of ChIP-seq data. By tet-repressible Myc system, we confirmed a Myc-dependent expression of IBTK in human B cells. Further, we showed that Ibtk loss affected the main apoptotic pathways dependent on Myc overexpression in pre-cancerous Eμ-myc mice, in particular, MCL-1 and p53. Of note, we found that loss of IBTK impaired cell cycle and increased apoptosis also in a human epithelial cell line, HeLa cells, in Myc-independent manner. Taken together, these results suggest that Ibtk sustains the oncogenic activity of Myc by inhibiting apoptosis of murine pre-cancerous B cells, as a cell-specific mechanism. Our findings could be relevant for the development of IBTK inhibitors sensitizing tumor cells to apoptosis.

| S-EPMC6459904 | biostudies-literature

Transgenic MYC OFF timecourse in murine MYC-dependent cell line

Project description:In this experiment we determine MYC-dependent changes in a MYC OFF time-course. Using the established 4188 cell line derived from the Eμ-tTA/Tet-O-MYC primary model of T-ALL, we performed RNA-seq at 0 (MYC ON), and 4, 8, 12, 24, and 48 hours after addition of 20ng/µl doxycycline (MYC OFF)

2021-07-01 | GSE178580 | GEO

Tristetraprolin is a tumor suppressor that impairs Myc-induced lymphoma and abolishes the malignant state [bone marrow B cells].

Project description:Myc oncoproteins directly regulate transcription by binding to target genes, yet this only explains a fraction of the genes affected by Myc. mRNA turnover is controlled via AU-binding proteins (AUBPs) that recognize AU-rich elements (AREs) found within many transcripts. Analyses of precancerous and malignant Myc-expressing B cells revealed that Myc regulates hundreds of ARE-containing (ARED) genes and select AUBPs. Notably, Myc directly suppresses transcription of Tristetraprolin (TTP/ZFP36), an mRNA-destabilizing AUBP, and this circuit is also operational during B lymphopoiesis and IL7 signaling. Importantly, TTP suppression is a hallmark of cancers with MYC involvement, and restoring TTP impairs Myc-induced lymphomagenesis and abolishes maintenance of the malignant state. Further, there is a selection for TTP loss in malignancy; thus, TTP functions as a tumor suppressor. Finally, Myc/TTP-directed control of select cancer-associated ARED genes is disabled during lymphomagenesis. Thus, Myc targets AUBPs to regulate ARED genes that control tumorigenesis. Wild type, Eµ-TTP-1, precancerous Eμ-Myc and precancerous Eμ-Myc;Eµ-TTP-1 transgenic bone marrow B cells (from 4-6 week old littermates; 94% C57BL/6) were investigated. These samples were used for subsequent RNA purification, labeling and hybridization to MOE430 2.0 Affymetrix arrays.

2012-08-01 | E-GEOD-33474 | biostudies-arrayexpress

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