ABSTRACT: Expression data from Hodgkin lymphoma cell lines L-428 and L-1236: L-428 and L-1236 cells were transduced with tGFP-EBF1 or as control tGFP-only.
Project description:The transcription factor network in Hodgkin lymphoma (HL) represents a unique composition of proteins found in no other hematopoietic cell. An aberrant downregulation of the B cell transcription factor EBF1 is observed in the B cell-derived Hodgkin and Reed/Sternberg (HRS) tumor cells. Herein, we elucidated the consequences of the down regulation of this factor in HL. To obtain a more comprehensive overview of EBF1 regulated genes in cHL cell lines, we performed a gene chip analysis comparing gene expression in tGFP-EBF1-transduced L-1236 and L-428 cells compared to samples transduced with vectors encoding only tGFP. 12 total samples were analyzed. Three independent samples were analyzed per condition and cell line.We generated the following pairwise comparisons using Bioconductor: tGFP-EBF1 L-428 < tGFP L-428; tGFP-EBF1 L-1236 < tGFP L-1236. Genes with an FDR≤ 5 % and a fold-change ≥ 2.0 and ≤ -2.0 were selected.
Project description:The transcription factor network in Hodgkin lymphoma (HL) represents a unique composition of proteins found in no other hematopoietic cell. An aberrant downregulation of the B cell transcription factor EBF1 is observed in the B cell-derived Hodgkin and Reed/Sternberg (HRS) tumor cells. Herein, we elucidated the consequences of the down regulation of this factor in HL. To obtain a more comprehensive overview of EBF1 regulated genes in cHL cell lines, we performed a gene chip analysis comparing gene expression in tGFP-EBF1-transduced L-1236 and L-428 cells compared to samples transduced with vectors encoding only tGFP.
Project description:Global proteomics profiling of anaplastic large cell lymphoma cell lines DEL, SU-DHL-1 (ALK+), Mac-1, Mac-2A (ALK-) as well as Hodgkin lymphoma cell lines L-428, L-540, L-1236 and HDLM-2.
Project description:Ophelia syndrome is characterized by the coincidence of severe neuropsychiatric symptoms, classical Hodgkin lymphoma, and the presence of antibodies to the metabotropic glutamate 5 receptor (mGluR5). Little is known about the pathogenetic link between these symptoms and the role anti-mGluR5-antibodies play. We investigated lymphoma tissue from patients with Ophelia syndrome and with isolated classical Hodgkin lymphoma by quantitative immunocytochemistry for mGluR5-expression. Further, we studied the L-1236, L-428, L-540, SUP-HD1, KM-H2, and HDLM-2 classical Hodgkin lymphoma cell lines by FACS and Western blot for mGluR5-expression, and by transcriptome analysis. mGluR5 surface expression differed significantly in terms of receptor density, distribution pattern, and percentage of positive cells. Highest levels were found in the L-1236 line. RNA-sequencing revealed more than 800 genes that were higher expressed in L-1236 in comparison to classical Hodgkin lymphoma-controls. High mGluR5-expression was associated with upregulation of PI3K/AKT and MAPK pathways and of downstream targets (e.g. EGR1) known to be involved in classical Hodgkin lymphoma progression. Finally, mGluR5 expression was increased in the classical Hodgkin lymphoma-tissue of our Ophelia syndrome patient in contrast to five classical Hodgkin lymphoma-patients without autoimmune encephalitis. Given the association of encephalitis and classical Hodgkin’s lymphoma in Ophelia syndrome, it is possible that mGluR5-expression on classical Hodgkin lymphoma cells not only drives tumor progression, but may also trigger anti-mGluR5 encephalitis already before classical Hodgkin lymphoma-manifestation.
Project description:The transcription factor network in Hodgkin lymphoma (HL) represents a unique composition of proteins found in no other hematopoietic cell. Among these factors, an aberrant expression of the T cell transcription factor GATA-3 is observed in the B cell-derived Hodgkin and Reed/Sternberg (HRS) tumor cells. Herein, we elucidated the regulation and function of this factor in HL To obtain a more comprehensive overview of GATA-3 regulated genes in cHL cell lines, we performed a gene chip analysis comparing gene expression in GATA-3-specific shRNA-transduced L-1236 and U-HO1 cells compared to samples transduced with vectors encoding scrambled shRNAs. 12 Total samples were analyzed. Three independent samples were analyzed per condition and cell line.We generated the following pairwise comparisons using Bioconductor: shRNA Gata-3 UHO-1 < control shRNA UHO-1; shRNA Gata-3 L1236 < control shRNA L-1236. Genes with an FDR≤ 25% and a fold-change ≥ 1.5 and ≤ -1.5 were selected.
Project description:The transcription factor network in Hodgkin lymphoma (HL) represents a unique composition of proteins found in no other hematopoietic cell. Among these factors, an aberrant expression of the T cell transcription factor GATA-3 is observed in the B cell-derived Hodgkin and Reed/Sternberg (HRS) tumor cells. Herein, we elucidated the regulation and function of this factor in HL To obtain a more comprehensive overview of GATA-3 regulated genes in cHL cell lines, we performed a gene chip analysis comparing gene expression in GATA-3-specific shRNA-transduced L-1236 and U-HO1 cells compared to samples transduced with vectors encoding scrambled shRNAs.
Project description:This SuperSeries is composed of the following subset Series: GSE25986: Gene expression profiling of cell lines derived from classical Hodgkin lymphoma GSE25987: Gene expression profiling of Hodgkin lymphoma cell line KMH2: Comparison of CIITA-BX648577 knockdown cultures with non-silencing controls GSE25989: Copy number analysis of Hodgkin lymphoma cell lines KM-H2 and L-428 Refer to individual Series *** This submission represents the microarray gene expression and microarray copy number components of the study
Project description:Persistent NF-κB activation is a hallmark of the malignant Hodgkin/Reed-Sternberg (HRS) cells in classical Hodgkin lymphoma (cHL). Analysis of the cHL cell-secreted key factors for NF-κB activation by chromatography and subsequent mass spectrometry revealed lymphotoxin-α (LTA) as the causative factor for autocrine and paracrine activation of canonical and noncanonical NF-κB in cHL cell lines. Upon CRISPR/Cas9-mediated gene knockout of LTA in the cell line L-1236, we performed expression analysis of LTA knockout versus control cells by using the Affymetrix array, Clariom S human, profiling tool.
Project description:Expression data from Hodgkin lymphoma cell lines UHO-1 and L-1236 transduced with shRNAs against GATA-3 or non-functional control shRNAs
Project description:Persistent activation of canonical and non-canonical NF-κB pathways is a hallmark of the malignant Hodgkin and Reed-Sternberg cells in classical Hodgkin lymphoma (cHL). We identified lymphotoxin alpha (LTA), which is secreted by the cHL cell line L-1236 in high concentrations. This cytokine contributes to the constitutive activation of the canonical and non-canonical NF-κB pathways. L-1236 cells were purchased from the DSMZ (Braunschweig, Germany) and cultured in RPMI (Gibco) with 10% heat-inactivated fetal calf serum (FCS; Gibco). Cells were transducted with the lentiCRIPSPR v2 vector containing gRNAs which target the second (g2) and the fourth exon (g3) of LTA. Following single cell clonal selection, L-1236 control cells (v2) and two LTA knockout (KO) clones g2_1 and g3_4 were cultured in normal culture medium for 72 h. The RNA was extracted using the RNeasy kit (Qiagen) according to manufacturer’s instructions. Preparation of cDNA, fragmentation and labeling was performed with the GeneChIPTM WT PLUS reagent kit (ThermoFisher Scientific). Samples were hybridized to the human Clariom™ S Assay (ThermoFisher Scientific).
