Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA196519 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Knock-down of BCL6 expression in human Diffuse Large B-Cell Lymphoma cell lines
2015-07-13 | E-GEOD-45838 | ExpressionAtlas
Project description:BCL6 is a key oncogene in lymphoma pathogenesis. The expression of BCL6 in lymphoid cells can be deregulated by several mechanisms, including chromosomal translocations, somatic mutations in the promoter regulatory regions or reduced proteasome-mediated degradation. FBXO11 was recently identified as a major ubiquitin ligase involved in the degradation of BCL6 and is frequently inactivated in diffuse large B-cell lymphoma (DLBCL). In this work, we found that FBXO11 is frequently mutated in Burkitt lymphoma (BL) but rarely mutated in other BCL6-positive lymphomas, such as follicular lymphoma (FL). All mutations tested impaired FBXO11 mediated BCL6 degradation and FBXO11 knock-out completely stabilized BCL6 levels in human BL cell lines. Conditional deletion of one copy or both copies of FBXO11 in c-Myc-driven B cell lymphoma in mice accelerated lymphomagenesis, genetically confirming that FBXO11 is a haplo-insufficient oncosuppressor in lymphoma. In both FBOX11 WT and deficient BL mouse and human cell lines, blockade of BCL6 via a specific degrader or BCL6 inhibitors, impaired lymphoma growth in vitro and in vivo, an effect further enhanced by co-inhibition of c-Myc activity. Overall these findings not only establish FBXO11 as one of the most frequently mutated genes in BL, but also elucidate its biological functions in lymphomagenesis and thereby identify BCL6 as a specific therapeutic target in BL.
2021-12-31 | GSE159303 | GEO
Project description:EZH2 mediates the humoral immune response and drives lymphomagenesis through de novo formation of bivalent chromatin domains and critical germinal center (GC) B cell promoters. We show that such formation is dependent on the presense of BCL6 and the presence of non-canonical PRC1-BCOR complex. We observe that BCL6 and EZH2 cooperate to accelerate diffuse large B cell lymphoma (DLBCL) development and combinatorial targeting of these repressors results in enhanced anti-lymphoma activity in vitro, in vivo, and in primary human DLBCLs. DLBCL cell lines treated with BCL6 inhibitor 79-6.1085
2016-07-20 | E-GEOD-73109 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE30357: Chip-chip from human diffuse large B cell lymphoma cell lines with IRF8 GSE30358: Mouse B cell lymphoma cell lines:IRF8 knockdown cells vs. Control GSE30519: Chip-chip from mouse diffuse large B cell lymphoma cell lines with IRF8 GSE30520: Chip-chip from mouse diffuse large B cell lymphoma cell lines with PU.1 Refer to individual Series
2011-10-14 | E-GEOD-30359 | biostudies-arrayexpress
Project description:Chip-chip from human diffuse large B cell lymphoma cell lines with IRF8
| PRJNA154813 | ENA
Project description:The multifunctional protein lipopolysaccharide-induced TNFalpha factor (LITAF) induces the secretion of inflammatory cytokines in monocytes and regulates protein degradation in neural cells. In B-cell lymphomas, LITAF is frequently inactivated by epigenetic mechanisms, but beyond these data little is known about its regulation and function. Immunohistochemical and gene expression profiling analyses of normal and malignant B-cells revealed that LITAF and BCL6 exhibited opposite expression patterns. Accordingly, chromatin immunoprecipitation and luciferase experiments showed that LITAF is transcriptionally repressed by BCL6 in germinal center (GC) lymphocytes and in B-cell lymphoma cells. Gain- and-loss-of-function assays demonstrated that LITAF does not exert any of its previous roles. Conversely, LITAF co-localized with autophagosomes in B-cells whereby activated autophagic responses, which were abrogated upon LITAF silencing. Therefore, BCL6-mediated transcriptional repression of LITAF may contribute to an appropriate GC reaction by suppressing autophagy in GC lymphocytes, whereas constitutive repression of autophagic responses may promote B-cell lymphoma development. 40 diffuse large B-cell lymphoma (DLBCL) and 3 splenic marginal zone lymphoma (SMZL) untreated cell lines were analyzed for global gene expression with the GeneChip® Human Genome U133 Plus 2.0 Array (Affymetrix). SMZL cell lines were hybridized in duplicate, resulting in a total of 46 microarrays.
2012-11-10 | E-GEOD-42203 | biostudies-arrayexpress
Project description:We have included human samples including bladder tissue, Cervical tissue, Colorectal tissue, diffuse large B-cell lymphoma, Gastric tissue, glioblastoma multiforme, K562 cell, thyroid tissue, Plasma, Leukemia, Sarcoma, squamous cell lung carcinoma, hepatocellular K562 cell lines. The details are described in Table 1 and Supplementary Table 1.
2019-11-11 | PXD015314 | iProX
Project description:EZH2 mediates the humoral immune response and drives lymphomagenesis through de novo formation of bivalent chromatin domains and critical germinal center (GC) B cell promoters. We show that such formation is dependent on the presense of BCL6 and the presence of non-canonical PRC1-BCOR complex. We observe that BCL6 and EZH2 cooperate to accelerate diffuse large B cell lymphoma (DLBCL) development and combinatorial targeting of these repressors results in enhanced anti-lymphoma activity in vitro, in vivo, and in primary human DLBCLs.
2016-07-20 | GSE73109 | GEO
Project description:The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. Tyrosine kinase inhibitors (TKI) are widely used to treat patients with leukemia driven by BCR-ABL1 and other oncogenic tyrosine kinases. In response to TKI-treatment, BCR-ABL1 ALL cells upregulate BCL6 protein levels by ~90-fold, i.e. to similar levels as in diffuse large B cell lymphoma (DLBCL) with BCL6 translocations. In this study, we used genome tiling arrays to identify BCL6 target genes with specific recruitment of BCL6. Three Ph+ ALL cell lines (BV-173, NALM-1 and TOM-1) in duplicate were either treated with 10µM STI571 (Imatinib) for 24 hours or cultured in absence of STI571.
2011-02-15 | E-GEOD-24404 | biostudies-arrayexpress