Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression profiling of FOXP1-silenced diffuse large B-cell lymphoma (DLBCL) cell lines

ABSTRACT: To identify differentially expressed genes regulated by FOXP1 in DLBCL cells via gene expression profiling of GCB-DLBCL (DB, K422) and ABC-DLBCL (OCI-Ly3, HBL-1) cell lines treated with siRNA targeting FOXP1 or non-silencing siRNA control. Two GCB-DLBCL (DB, K422) and two ABC-DLBCL (OCI-Ly3, HBL-1) cell lines were each treated separately with two independent siRNA oligonucleotides targeting FOXP1 (siFOXP1_308, siFOXP1_309) or non-silencing siRNA (siCtrl). Biological replicates derived from three independent experiments were obtained, RNA-extracted and subsequently hybridized into a human microarray platform for gene expression profiling.

ORGANISM(S): Homo sapiens

SUBMITTER: Kah Keng Wong

PROVIDER: E-GEOD-71526 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The activated B cell-like (ABC) subgroup of diffuse large B cell lymphoma (DLBCL) is characterized by constitutive activation of the NF-ÃªB pathway. Here we show that the NF- ÃªB pathway induces the expression of the cytokines IL-6 and IL-10 in ABC DLBCL cell lines, which also have high levels of total and phosphorylated STAT3 protein, suggesting autocrine signaling. Using RNA interference for STAT3, we defined a gene expression signature of IL-6 and IL-10 signaling through STAT3. Based on this signature, we constructed a molecular predictor of STAT3 signaling that defined a subset of ABC DLBCL tumors with high expression of STAT3, IL-6 and/or IL-10, and their downstream targets. Although the STAT3-high and STAT3-low subsets had equivalent expression of genes that distinguish ABC DLBCL from GCB DLBCL, STAT3-high ABC DLBCLs had higher expression of signatures that reflected NF-kB activity, proliferation, and glycolysis. A smallmolecule inhibitor of JAK signaling, which blocked STAT3 signature expression, was toxic only for ABC DLBCL lines, and synergized with an inhibitor of NF-kB signaling. These findings suggest that the biological interplay between the STAT3 and NF-kB pathways may be exploited for the treatments of a subset of ABC DLBCLs. Activated B cell-like (ABC) subgroup of diffuse large B cell lymphoma (DLBCL) cell lines were used as model systems to study the cytokine pathways in these cells. We expressed inducible IkB super-repressor for 1 to 24 hours to identify NF-kB target genes in OCI-Ly3 and OCI-Ly10 cells for a total of 13 arrays with replicates of each time point. We treated OCI-Ly3 cells with IL-10 for 1 to 96 hours for a total of 10 arrays with replicates of each time point. We treated OCI-Ly10 cells with IL-6 for 30 minutes to 24 hours for a total of 8 arrays with replicates of each time point. OCI-Ly10 cells transfected with no siRNA versus STAT3-siRNA for 8, 24, or 48 hours for a total of 5 arrays with replicates for 24 and 48 hours. We treated OCI-Ly10 cells with JAK inhibitor I for 3 and 6 hours for a total of 4 arrays with replicates of each time point.

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Gene expression profiling of FOXP1-silenced diffuse large B-cell lymphoma (DLBCL) cell lines

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