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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

Histone deacetylase 1 plays a predominant pro-oncogenic role in Eμ-myc driven B cell lymphoma.

Project description:The two histone deacetylases (Hdacs), Hdac1 and Hdac2, are erasers of acetylation marks on histone tails, and are important regulators of gene expression that were shown to play important roles in hematological malignancies. However, several recent studies reported opposing tumor-suppressive or tumor-promoting roles for Hdac1 and Hdac2. Here, we investigated the functional role of Hdac1 and Hdac2 using the Eμ-myc mouse model of B cell lymphoma. We demonstrate that Hdac1 and Hdac2 have a pro-oncogenic role in both Eμ-myc tumorigenesis and tumor maintenance. Hdac1 and Hdac2 promote tumorigenesis in a gene dose-dependent manner, with a predominant function of Hdac1. Our data show that Hdac1 and Hdac2 impact on Eμ-myc B cell proliferation and apoptosis and suggest that a critical level of Hdac activity may be required for Eμ-myc tumorigenesis and proper B cell development. This provides the rationale for utilization of selective Hdac1 and Hdac2 inhibitors in the treatment of hematological malignancies.

| S-EPMC5122906 | biostudies-literature

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

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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

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