Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

ChIP-on-chip of BCL6

ABSTRACT: Identification BCL6 target genes in primary germinal center cells and DLBCL cell lines by ChIP-on-chip Three replicates in each type of cells

ORGANISM(S): Homo sapiens

SUBMITTER: weimin ci

PROVIDER: E-GEOD-15179 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

The BCL6 transcriptional program features repression of multiple oncogenes in primary B cells and is deregulated in DLBCL.

Ci Weimin W Polo Jose M JM Cerchietti Leandro L Shaknovich Rita R Wang Ling L Yang Shao Ning SN Ye Kenny K Farinha Pedro P Horsman Douglas E DE Gascoyne Randy D RD Elemento Olivier O Melnick Ari A

Blood 20090323 22

The BCL6 transcriptional repressor is required for development of germinal center (GC) B cells and when expressed constitutively causes diffuse large B-cell lymphomas (DLBCLs). We examined genome-wide BCL6 promoter binding in GC B cells versus DLBCLs to better understand its function in these settings. BCL6 bound to both distinct and common sets of functionally related gene in normal GC cells versus DLBCL cells. Certain BCL6 target genes were preferentially repressed in GC B cells, but not DLBCL ...[more]

PMID: 19307668

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Project description:BACKGROUND & AIMS: C/EBPbeta is involved in numerous process as carcinogenesis but its role is still not clear due to the existence of an active form (LAP) and an inhibitory form (LIP) of this transcription factor. The main goals of the present research were (i) the identification of genes inversely regulated by LAP and LIP i-e the genuine C/EBPbeta molecular signature in the Hep3B human hepatoma cell line (ii) a better understanding of LAP and LIP respective role in hepatic cells survival and proliferation (iii) the search of the C/EBPbeta signature among hepatocellular carcinomas. METHODS: Using Tet-off expression system we engineered Hep3BLAP and Hep3BLIP cells, in which LAP and LIP were over-expressed respectively. Then, using both expression profiling (DNA arrays) and ChIP-on-chip analysis, we identified genes inversely and/or directly regulated by each of the C/EBPbeta isoforms. The expression levels of these genes regulated by LAP/LIP were compared in controls and HCCs patients. RESULTS: We identified 676 genes inversely regulated by LAP and LIP and among these, 45 are direct targets. Using functional studies, we displayed the opposite role of LAP and LIP in staurosporine-induced cell death and the implication of LAP in the repression of Hep3B cells proliferation. Finally we identified a subgroup of HCCs with a deregulation of 165 genes belonging to C/EBPbeta signature and coding for proteins involved in chemoresistance and metastasis formation. CONCLUSIONS: Our study increases knowledge on LAP and LIP functions and provides first evidence that their molecular signature in the HCCs could predict tumor evolution. Total genomic DNA were extracted from 3 Hep3BLAP expressing LAP and were labelled Cy3 fluorochrome. Genomic DNA were extracted from 3 Hep3BLAP expressing LAP, were immunoprecipited with anti-CEBPbeta antibody and were labelled with Cy5 fluorochrome. Each sample was hybridized on an Agilent two-color microarray G4489A (Human Promoter ChIP-on-Chip Set 244K).

Dataset Information

ChIP-on-chip of BCL6

Publications

The BCL6 transcriptional program features repression of multiple oncogenes in primary B cells and is deregulated in DLBCL.

Similar Datasets

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