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PRDM11 ChIP in U2932 cells

ABSTRACT: The PR-domain family e(PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We found that loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Moreover, we show that patients with PRDM11-deficient diffuse large B cell lymphomas (DLBCLs) have poorer overall survival and belong to the non-Germinal Center B cell (GCB)-like subtype. Mechanistically, genome-wide mapping of PRDM11 binding sites coupled with transcriptome sequencing in human DLBCL cells evidenced that PRDM11 associates with transcriptional start sites of target genes and regulates important oncogenes such as FOS and JUN. Hence, we characterize PRDM11 as a novel tumor suppressor controlling the expression of key oncogenes and add new mechanistic insight into B-cell lymphomagenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE56064 | GEO | 2015/03/02

SECONDARY ACCESSION(S): PRJNA242327

REPOSITORIES: GEO

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PRDM11 ChIP in U2932 cells

Project description:The PR-domain family e(PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We found that loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Moreover, we show that patients with PRDM11-deficient diffuse large B cell lymphomas (DLBCLs) have poorer overall survival and belong to the non-Germinal Center B cell (GCB)-like subtype. Mechanistically, genome-wide mapping of PRDM11 binding sites coupled with transcriptome sequencing in human DLBCL cells evidenced that PRDM11 associates with transcriptional start sites of target genes and regulates important oncogenes such as FOS and JUN. Hence, we characterize PRDM11 as a novel tumor suppressor controlling the expression of key oncogenes and add new mechanistic insight into B-cell lymphomagenesis. 5 samples: PRDM11 Ab1, PRDM11 Ab2, RNA Polymerase II, IgG and input

2015-03-02 | E-GEOD-56064 | biostudies-arrayexpress

Effect of PRDM11 depletion in U2932 cells

2015-03-02 | E-GEOD-56235 | biostudies-arrayexpress

Effect of PRDM11 depletion in U2932 cells

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Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors

Project description:The PR-domain family (PRDMs) encodes transcriptional regulators, several of which are deregulated in cancer. We found that loss of Prdm11 accelerates MYC-driven lymphomagenesis in the Eµ-Myc mouse model. Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors to identify genes deregulated by loss of Prdm11

2015-03-02 | GSE56063 | GEO

Expression data from EμMyc;Prdm11 WT and EμMyc;Prdm11 KO end-stage splenic tumors

2015-03-02 | E-GEOD-56063 | biostudies-arrayexpress

Transcription profiling of mouseB-cell lymphomas with defined genetic alterations in p53 or p73

Project description:Induction of apoptosis by the tumor suppressor p53 is known to protect from Myc-driven lymphomagenesis. The p53 family member p73 is also a pro-apoptotic protein, which is activated in response to oncogenes like Myc. We therefore investigated whether p73 provides a similar protection from Myc-driven lymphomas as p53. To generate B-cell lymphomas with defined genetic alterations in p53 or p73, we crossed the Eµ-Myc transgenic to mice heterozygous for germ-line deletions in p53 (p53+/) or p73 (p73+/-). Lymphomas which have spontaneously developed in Eµ-Myc transgenic animals with the genotypes p53+/+, p53+/-, p73+/+, p73+/- or p73-/- were isolated when the animals were moribund and further processed for gene expression profiling with 22.5K cDNA microarrays.

2008-12-05 | E-MEXP-1620 | biostudies-arrayexpress

PTEN loss defines a PI3K/AKT pathway-dependent germinal center subtype of diffuse large B-cell lymphoma

Project description:Diffuse large B-cell lymphoma (DLBCL) represents a heterogeneous diagnostic category with distinct molecular subtypes that can be defined by gene expression profiling. However, even within these defined subtypes, heterogeneity prevails. To further elucidate the pathogenesis of these entities, we determined the expression of the tumor suppressor phosphatase and tensin homolog (PTEN) in 248 primary DLBCL patient samples. These analyses revealed that loss of PTEN was detectable in 55% of germinal center B-cell-like (GCB) DLBCLs, whereas this abnormality was found in only 14% of non-GCB DLBCL patient samples. In GCB DLBCL, the PTEN status was inversely correlated with activation of the oncogenic PI3K/ protein kinase B (AKT) pathway in both DLBCL cell lines and primary patient samples. Re-expression of PTEN induced cytotoxicity in PTEN-deficient GCB DLBCL cell line models by inhibiting PI3K/AKT signaling, indicating an addiction to this pathway in this subset of GCB DLBCLs. PI3K/AKT inhibition induced down-regulation of the transcription factor MYC. Re-expression of MYC rescued GCB DLBCL cells from PTEN-induced toxicity, identifying a regulatory mechanism of MYC expression in DLBCL. Finally, pharmacologic PI3K inhibition resulted in toxicity selectively in PTEN-deficient GCB DLBCL lines. Collectively, our results indicate that PTEN loss defines a PI3K/ AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that pharmacologic inhibition of PI3K might represent a promising therapeutic approach in these lymphomas.

2013-07-09 | GSE45495 | GEO

CRISPRi screen identifies core regions in IGH enhancers essential for non-Hodgkin lymphoma cells survival

Project description:Chromosomal translocations in non-Hodgkin lymphoma (NHL) are known to bring oncogenes (e.g. MYC, BCL2) under the regulation of immunoglobulin heavy chain (IGH) super-enhancers, composed of the intronic Eµ enhancer and 3’ regulatory regions (3’RR1, 3’RR2). Deregulation of translocated oncogenes by enhancer activity can contribute to lymphomagenesis. The role of IGH enhancers in normal B-cell development is well established, but the knowledge regarding precise mechanisms of their involvement in control of the translocated oncogenes is limited. We previously identified exact regions within IGH regulatory elements, one in the Eµ and two in each of the 3'RRs, whose targeting profoundly inhibited NHL cells growth. The goal of this project was to reveal enhancer RNAs (eRNA) transcribed from Eµ and 3'RRs and their essential regions. With the use of chromatin-enriched RNA-Seq we confirmed bi-directional transcription from those core enhancer regions and further validated eRNAs expression in a large panel of NHL cell lines and in patient-derived samples. We showed in several NHL cell lines that CRISPR/dCas9-KRAB-mediated inhibition of essential IGH enhancer regions decreased expression of eRNAs and translocated oncogenes in the fashion likely related to their breakpoints pattern within IGH locus. Our results provide new insights into the current understanding of IGH enhancers role in B-cell NHLs.

2024-06-10 | GSE247393 | 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

PTEN loss deM-oM-,M-^Anes a PI3K/AKT pathway-dependent germinal center subtype of diffuse large B-cell lymphoma

Project description:Diffuse large B-cell lymphoma (DLBCL) represents a heterogeneous diagnostic category with distinct molecular subtypes that can be deM-oM-,M-^Aned by gene expression proM-oM-,M-^Aling. However, even within these deM-oM-,M-^Aned subtypes, heterogeneity prevails. To further elucidate the pathogenesis of these entities, we determined the expression of the tumor suppressor phosphatase and tensin homolog (PTEN) in 248 primary DLBCL patient samples. These analyses revealed that loss of PTEN was detectable in 55% of germinal center B-cell-like (GCB) DLBCLs, whereas this abnormality was found in only 14% of non-GCB DLBCL patient samples. In GCB DLBCL, the PTEN status was inversely correlated with activation of the oncogenic PI3K/ protein kinase B (AKT) pathway in both DLBCL cell lines and primary patient samples. Reexpression of PTEN induced cytotox- icity in PTEN-deM-oM-,M-^Acient GCB DLBCL cell line models by inhibiting PI3K/AKT signaling, indicating an addiction to this pathway in this subset of GCB DLBCLs. PI3K/AKT inhibition induced down-regulation of the transcription factor MYC. Reexpression of MYC rescued GCB DLBCL cells from PTEN-induced toxicity, identifying a regulatory mechanism of MYC expression in DLBCL. Finally, pharmacologic PI3K inhibition resulted in toxicity selectively in PTEN-deM-oM-,M-^Acient GCB DLBCL lines. Collectively, our results indicate that PTEN loss deM-oM-,M-^Anes a PI3K/ AKT-dependent GCB DLBCL subtype that is addicted to PI3K and MYC signaling and suggest that pharmacologic inhibition of PI3K might represent a promising therapeutic approach in these lymphomas. This GEO dataset is comprised of a) GEP measurements for 34 primary DLBCL patient samples plus two reference samples, b) 8 paired GEP measurements of the HT DLBCL cell line and c) aCGH measurements for two DLBCL cell lines in addition to previously published cell lines in GSE43272 (i.e., Sample GSM1059798). All of these data were used in the paper cited below.

2013-07-09 | E-GEOD-45495 | biostudies-arrayexpress

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