Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-10821
PROVIDER: PRJNA107437 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:LMP1 mediated gene expression changes in transfected CD10+ GC B cells
| PRJNA107423 | ENA
Project description:KDM6B-induced gene expression changes in transfected CD10-positive GC B cells
| PRJNA130345 | ENA
Project description:Hodgkin lymphoma (HL) is a malignancy of germinal center (GC) B-cell origin. To explore the role of long non-coding RNAs (lncRNAs) in HL, we studied lncRNA expression patterns in normal B-cell subsets, HL cell lines and tissues. Naive and memory B-cells showed a highly similar lncRNA expression pattern, distinct from GC-B cells. Significant differential expression between HL and normal GC-B cells was observed for 475 lncRNA loci. For two validated lncRNAs an enhanced expression was observed in HL, diffuse large B cell lymphoma and lymphoblastoid cell lines. For a third lncRNA, increased expression levels were observed in HL and part of Burkitt lymphoma cell lines. RNA-FISH on primary HL tissues revealed a tumor cell-specific expression pattern for all three lncRNAs. A potential cis-regulatory role was observed for 107 differentially expressed lncRNA-mRNA pairs localizing within a 60kb region. In line with a cis-acting role, we showed a preferential nuclear localization for two selected candidates. Thus, we showed dynamic lncRNA expression changes during the transit of normal B-cells through the GC reaction and widely deregulated lncRNA expression patterns in HL. Three lncRNAs showed a tumor cell-specific expression pattern in HL tissues and might therefore be of value as a biomarker.
2016-05-26 | GSE81086 | GEO
Project description:ATAC-seq in sorted GC centroblasts (GCB: CD20+CD44-CD10+CXCR4+), GC centrocytes (CC: CD20+CD44-CD10+CXCR4-), naïve B cells (NB: CD20+CD44+CD10-IgD+), memory B cells (MB: CD20+CD44+CD10-CD38-CD27+), and plasma cells (PC: CD20+CD44+CD10-CD38+CD27+)
2021-08-03 | GSE159314 | GEO
Project description:Gene expression was compared between four B-cell derived HL cell lines (L428, L1236, L591, KMH2) and GC B cells from three different patients. Experiment Overall Design: Gene expression was compared between four B-cell derived HL cell lines (L428, L1236, L591, KMH2) and GC B cells from three different patients.
2008-10-26 | E-GEOD-10831 | biostudies-arrayexpress
Project description:Cell differentiation is associated with changes in chromatin organization and gene expression. In this study, we examine chromatin structure following differentiation of the human myeloid leukemia cell line (HL-60/S4) into granulocytes with retinoic acid (RA) or into macrophage with phorbol ester (TPA). We performed ChIP-seq of histone H3 and its modifications, analyzing changes in nucleosome occupancy, nucleosome repeat length, eu-/heterochromatin redistribution and properties of epichromatin (surface chromatin adjacent to the nuclear envelope). Nucleosome positions changed genome-wide, exhibiting a specific class of alterations involving nucleosome loss in extended (~1kb) regions, pronounced in enhancers and promoters. Genes that lost nucleosomes at their promoters showed a tendency to be upregulated. On the other hand, nucleosome gain was not systematic at functional elements and did not show simple effects on transcript levels. The average genome-wide nucleosome repeat length (NRL) did not change significantly with differentiation. However, we detected an approximate 10 bp NRL decrease around the hematopoietic transcription factor (TF) PU.1 and the architectural protein CTCF, suggesting an effect on NRL proximal to TF binding sites. Nucleosome occupancy changed in regions associated with H3K4me3 in differentiated cells, compared to untreated HL-60/S4 cells. Epichromatin regions, largely unaffected by cell differentiation, revealed an increased GC content and high nucleosome density compared to surrounding chromatin. Epichromatin showed depletion of major (permissive and repressive) histone modifications and revealed enrichment with PML body-associated genes. In general, chromatin changes during HL-60/S4 differentiation appeared to be more localized, compared to changes among diverse cell types studied elsewhere, suggesting that the cell lineage differentiation of HL-60/S4 cells involves less drastic nucleosome repositioning.
2017-04-27 | GSE90992 | GEO
Project description:Gene expression was compared between four B-cell derived HL cell lines (L428, L1236, L591, KMH2) and GC B cells from three different patients. Keywords: Cell type comparison
2008-10-10 | GSE10831 | GEO
Project description:LMP2A mediated gene expression changes in transfected CD10+ GCB cells
| PRJNA197359 | ENA
Project description:Micro (mi)RNAs not only play important roles in biological processes such as proliferation, metabolism, differentiation and apoptosis, but also in diseases such as cancers. We identified miRNAs with deregulated expression in Hodgkin lymphoma (HL) and investigated their role in the pathogenesis of HL. Small RNA sequencing revealed 84 significantly differentially expressed miRNAs in HL cell lines as compared to GC-B cells. Three upregulated miRNAs, miR-23a-3p, miR-24-3p and miR-27a-3p, were derived from one primary-miRNA transcript. Loss-of-function analysis for these miRNAs and their seed family members resulted in decreased growth upon miR-24-3p inhibition in three and of miR-27a/b-3p inhibition in one HL cell line. Apoptosis analysis indicated that the effect of miR-24-3p on cell growth is at least in part caused by an increase of apoptotic cells. Argonaute 2 (Ago2)-IP revealed 1,142 genes consistently targeted by miRNAs in at least three out of four HL cell lines. Furthermore, 52 out of the 1,142 genes were predicated targets of miR-24-3p. Functional annotation analysis revealed a function related to cell growth, cell death and/or apoptosis for 15 out of the 52 genes. Western blotting of the top-5 genes showed increased protein levels upon miR-24-3p inhibition for CDKN1B and MYC. In summary, we showed that miR-24-3p is upregulated in HL and its inhibition impaired cell growth possibly via targeting CDKN1B and MYC.
2017-02-26 | GSE92616 | GEO