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MicroRNA-24-3p is overexpressed in Hodgkin lymphoma and protects Hodgkin and Reed-Sternberg cells from apoptosis

ABSTRACT: MicroRNA-24-3p is overexpressed in Hodgkin lymphoma and protects Hodgkin and Reed-Sternberg cells from apoptosis

PROVIDER: PRJNA358165 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5121480.fastq.gz	Fastqsanger.gz
	SRR5121481.fastq.gz	Fastqsanger.gz
	SRR5121482.fastq.gz	Fastqsanger.gz
	SRR5121483.fastq.gz	Fastqsanger.gz
	SRR5121484.fastq.gz	Fastqsanger.gz

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MicroRNA-24-3p is overexpressed in Hodgkin lymphoma and protects Hodgkin and Reed-Sternberg cells from apoptosis [ChIP-chip]

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 | GSE92615 | GEO

MicroRNA-24-3p is overexpressed in Hodgkin lymphoma and protects Hodgkin and Reed-Sternberg cells from apoptosis [small RNA-Seq]

2017-02-26 | GSE92616 | GEO

Gene expression profiling of cell lines derived from classical Hodgkin lymphoma

Project description:Hodgkin lymphoma is derived from germinal center / post-germinal center B cells. To determine differentially expressed genes between Hodgkin Reed Sternberg cells and their presumed cell of origin we investigated the expression profiles of 5 commonly used Hodgkin lymphoma cell lines as compared to reactive germinal centers.

2010-12-11 | E-GEOD-25986 | biostudies-arrayexpress

Tumor infiltrating HLA-matched CD4+ T cells retargeted against Hodgkin and Reed-Sternberg cells

Project description:Hodgkin's lymphoma (HL) is one of the most frequent hematological malignancies. Due to its extraordinary composition, few tumor cells surrounded by a reactive infiltrate, HL can be seen as an ideal model system for research focusing on tumor immunology. In fact, the tumor cells of HL, so called Hodgkin/Reed-Sternberg (HRS) cells attract CD4+ T cells, which then build rosettes with the HRS cells. HRS cells further modulate the tumor microenvironment with the help of CD4+ T cells to avoid tumor rejection. Here, we mimicked this scenario using compatible CD4+ T cells receiveing data of profound interactions for the first time, as former studies were performed with allogeneic donors. Finally, we genetically retargeted compatible CD4+ T cells to kill HRS cells.

2016-11-29 | GSE75267 | GEO

Analyzing primary Hodgkin and Reed-Sternberg cells to capture the molecular and cellular pathogenesis of classical Hodgkin lymphoma

Project description:The pathogenesis of classical Hodgkin lymphoma (cHL), the most common lymphoma in the young, is still enigmatic, largely because its Hodgkin and Reed-Sternberg (HRS) tumor cells are rare in the involved lymph node and therefore difficult to analyze. Here, by overcoming this technical challenge and performing for the first time a genome-wide transcriptional analysis of microdissected HRS cells in comparison to other B-cell lymphomas, cHL lines and normal B-cell subsets, we show that they differ extensively from the usually studied cHL cell lines, that the lost B-cell identity of cHLs is not linked to the acquisition of a plasma cell-like gene expression program, and that Epstein-Barr virus infection of HRS cells has a minor transcriptional influence on the established cHL clone. Moreover, although cHL appears a distinct lymphoma entity overall, HRS cells of its histological subtypes diverged in their similarity to other related lymphomas. Unexpectedly, we identified two molecular subgroups of cHL associated to differential strengths of the transcription factor activity of the NOTCH1, MYC and IRF4 proto-oncogenes. Finally, HRS cells display deregulated expression of several genes potentially highly relevant to lymphoma pathogenesis, including silencing of the apoptosis-inducer BIK and of INPP5D, an inhibitor of the PI3K-driven oncogenic pathway. The present study complements the GSE12453 and GSE14879 records by adding the following 10 samples: 5 primary tumor samples and 5 cell line samples. The 5 primary tumor samples represent 1000-2000 neoplastic cells microdissected from frozen biopsies of 5 cases of primary mediastinal B-cell lymphoma (PMBL). The 5 cell line samples represent 500-1000 living neoplastic cells isolated by fluorescence-activated cell sorting from growing cultures of the classical Hodgkin lymphoma (cHL) cell lines L1236, L428, KMH2 and HDLM2 and the lymphocyte-predominant Hodgkin lymphoma (lpHL) cell line DEV.

2012-09-17 | E-GEOD-40160 | biostudies-arrayexpress

Analyzing primary Hodgkin and Reed-Sternberg cells to capture the molecular and cellular pathogenesis of classical Hodgkin lymphoma

2012-09-17 | GSE40160 | GEO

Fibroblasts in Nodular Sclerosing Classical Hodgkin Lymphoma Are Defined by a Specific Phenotype and Protect Tumor Cells From Brentuximab-Vedotin Induced Injury

Project description:Several studies have described a crosstalk between the tumour cells of cHL, the Hodgkin- and Reed-Sternberg (HRS) cells, and cancer-associated fibroblasts (CAF). However, to date a deep molecular characterization of these fibroblasts is lacking. Aim of the present study therefore was a comprehensive characterization of these fibroblasts.

2020-06-30 | GSE153517 | GEO

Characterization of human CD30+ B cells and their relationship to Hodgkin and Reed-Sternberg cells of Hodgkin lymphoma

Project description:Small subsets of B cells in the germinal center (GC) and in extrafollicular regions of lymph nodes express the activation marker CD30. Very little is known about the specific features of these cells and their relationship to the CD30-expressing Hodgkin and Reed/Sternberg (HRS) cells of Hodgkin lymphoma. Phenotypic and immunoglobulin V gene analyses revealed that CD30+ GC B lymphocytes represent typical GC B cells, and that CD30+ non-GC B cells are mostly post-GC B cells. However, despite these seemingly distinct identities, both CD30+ subsets share an unexpectedly large overlap in specific transcriptome patterns, and are strikingly different from bulk GC B cells and classical memory and plasma cells, respectively. A main common feature of these CD30+ B cells is a strong MYC signature. CD30+ GC B cells appear to represent the recently described MYC+ GC B cell subset of recirculating centrocytes at the stage of centroblast transition. CD30+ non-GC B cells rather represent highly activated and proliferating memory B cells, differentiating into plasma cells. Notably, CD30+ B cells were more similar in their transcriptome patterns to HRS cells than any other B cell subset investigated, suggesting that HRS cells may either derive from CD30+ B cells or acquired a similar activation signature. In comparison to CD30+ B cells and other lymphomas, HRS cells show a remarkable downregulation of genes regulating cell cycle, genomic stability and polyploidity, providing a potential explanation for the genomic instability and multinuclearity of HRS cells.

2018-06-13 | GSE83441 | GEO

Effect of lestaurtinib on KM-H2 HRS cell line

Project description:Effect of the tyrosine kinase inhibitor (TKI) lestaurtinib on Hodgkin and Reed/Sternberg (HRS) cell line KM-H2 compared to the solvent treated control.

2012-02-21 | E-MEXP-3565 | biostudies-arrayexpress

MicroRNA-24-3p is overexpressed in Hodgkin lymphoma and protects Hodgkin and Reed-Sternberg cells from apoptosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-02-26 | GSE92617 | GEO