Role of early B-cell factor 1 (EBF1) in Hodgkin lymphoma

A hallmark of classical Hodgkin lymphoma (cHL) is that the B-cell-derived Hodgkin and Reed–Sternberg (HRS) tumor cells have largely lost the B-cell-typical gene expression program. The factors causing this ‘reprogramming’ of HRS cells are only partly understood. As early B-cell factor 1 (EBF1), a ma...

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Veröffentlicht in:Leukemia 2013-03, Vol.27 (3), p.671-679
Hauptverfasser: Bohle, V, Döring, C, Hansmann, M-L, Küppers, R
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creator Bohle, V
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Hansmann, M-L
Küppers, R
description A hallmark of classical Hodgkin lymphoma (cHL) is that the B-cell-derived Hodgkin and Reed–Sternberg (HRS) tumor cells have largely lost the B-cell-typical gene expression program. The factors causing this ‘reprogramming’ of HRS cells are only partly understood. As early B-cell factor 1 (EBF1), a major B-cell transcription factor, is downregulated in HRS cells, we analyzed whether this downregulation contributes to the lost B-cell phenotype and tested the consequences of EBF1 re-expression in cHL cell lines. EBF1 re-expression caused an upregulation of B-cell genes, such as CD19 , CD79A and CD79B , although the B-cell genes FOXO1 and PAX5 remained lowly expressed. The re-expression of CD19 , CD79A and CD79B occurred largely without demethylation of promoter CpG motifs of these genes. In the cHL cell line L-1236 fitness decreased after EBF1 re-expression. These data show that EBF1 has the ability to reintroduce part of the B-cell signature in cHL cell lines. Loss of EBF1 expression in HRS cells therefore contributes to their lost B-cell phenotype. Notably, in the cHL cell line KM-H2 destructive mutations were found in one allele of EBF1 , indicating that genetic lesions may sometimes have a role in impairing EBF1 expression.
doi_str_mv 10.1038/leu.2012.280
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The factors causing this ‘reprogramming’ of HRS cells are only partly understood. As early B-cell factor 1 (EBF1), a major B-cell transcription factor, is downregulated in HRS cells, we analyzed whether this downregulation contributes to the lost B-cell phenotype and tested the consequences of EBF1 re-expression in cHL cell lines. EBF1 re-expression caused an upregulation of B-cell genes, such as CD19 , CD79A and CD79B , although the B-cell genes FOXO1 and PAX5 remained lowly expressed. The re-expression of CD19 , CD79A and CD79B occurred largely without demethylation of promoter CpG motifs of these genes. In the cHL cell line L-1236 fitness decreased after EBF1 re-expression. These data show that EBF1 has the ability to reintroduce part of the B-cell signature in cHL cell lines. Loss of EBF1 expression in HRS cells therefore contributes to their lost B-cell phenotype. 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Notably, in the cHL cell line KM-H2 destructive mutations were found in one allele of EBF1 , indicating that genetic lesions may sometimes have a role in impairing EBF1 expression.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>23174882</pmid><doi>10.1038/leu.2012.280</doi><tpages>9</tpages></addata></record>
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subjects 631/208/199
631/250/1619/40
631/45/612/822
692/699/67/1990/291/1556
Apoptosis
B cells
B-Lymphocytes - metabolism
B-Lymphocytes - pathology
Base Sequence
Biomarkers, Tumor - genetics
Biomarkers, Tumor - metabolism
Blotting, Western
Cancer Research
CD19 antigen
Cell Proliferation
Cells
CpG Islands
Critical Care Medicine
Demethylation
DNA Methylation
Early B-cell factor
Epigenetics
FOXO1 protein
Gene expression
Gene Expression Profiling
Gene Expression Regulation, Neoplastic
Genes
Genetic aspects
Genotype & phenotype
Hematology
Hodgkin Disease - genetics
Hodgkin Disease - metabolism
Hodgkin Disease - pathology
Hodgkin's disease
Hodgkin's lymphoma
Humans
Intensive
Internal Medicine
Leukemia
Lymphocytes B
Lymphoma
Medical research
Medicine
Medicine & Public Health
Methylation
Molecular Sequence Data
Mutation
Oligonucleotide Array Sequence Analysis
Oncology
original-article
Pax5 protein
Phenotypes
Physiological aspects
Promoter Regions, Genetic
Real-Time Polymerase Chain Reaction
Reed-Sternberg Cells - metabolism
Reed-Sternberg Cells - pathology
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - genetics
Sequence Homology, Nucleic Acid
Trans-Activators - genetics
Trans-Activators - metabolism
Transcription factors
Tumor cells
title Role of early B-cell factor 1 (EBF1) in Hodgkin lymphoma
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