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MiRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

ABSTRACT: miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. 16 CLL patients (8 Pre samples, 15 Ctrl samples, 15 IL-4 samples), 3 NBC (3 Ctrl samples, 3 IL-4 samples)

ORGANISM(S): Homo sapiens

SUBMITTER: Antonio Parrado

PROVIDER: E-GEOD-62137 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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IL-4 Up-Regulates MiR-21 and the MiRNAs Hosted in the CLCN5 Gene in Chronic Lymphocytic Leukemia.

Ruiz-Lafuente Natalia N Alcaraz-García María-José MJ Sebastián-Ruiz Silvia S García-Serna Azahara-María AM Gómez-Espuch Joaquín J Moraleda José-María JM Minguela Alfredo A García-Alonso Ana-María AM Parrado Antonio A

PloS one 20150424 4

Interleukin 4 (IL-4) induces B-cell differentiation and survival of chronic lymphocytic leukemia (CLL) cells. MicroRNAs (miRNAs) regulate mRNA and protein expression, and several miRNAs, deregulated in CLL, might play roles as oncogenes or tumor suppressors. We have studied the miRNA profile of CLL, and its response to IL-4, by oligonucleotide microarrays, resulting in the detection of a set of 129 mature miRNAs consistently expressed in CLL, which included 41 differentially expressed compared t ...[more]

PMID: 25909590

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Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

Project description:Gene expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples. Patient CLL01 was also treated with IL-4 plus 5 mg/ml ERK activation inhibitor peptide I, or IL-4 plus 10 ÂµM NFkB activation inhibitor, and IL-4 plus 100 mg/ml cyclic-pifithrin-Î± 23 CLL patients (10 Pre samples, 23 Ctrl samples, 23 IL-4 samples, 1 IL-4 plus ERK inhibitor sample, 1 IL-4 plus NFkB inhibitor sample, 1 IL-4 plus Pifithrin sample), 13 NBC (10 Pre samples, 10 Ctrl samples, 13 IL-4 samples)

2014-10-06 | E-GEOD-55288 | biostudies-arrayexpress

miRNA regulation by interleukin-4 (IL-4) in chronic lymphocytic leukemia (CLL)

Project description:miRNA expression profiles of CLL cells and normal B cells (NBC) treated for 18 hr with 10 ng/ml IL-4, compared with culture with nothing (Ctrl) and the basal (Pre) samples.

2015-06-15 | GSE62137 | GEO

Identification of interleukin-4 (IL-4) targets in chronic lymphocytic leukemia (CLL)

2014-10-06 | GSE55288 | GEO

Gene signature of CLL cells cultured with activated T cells or CD40L-expressing cells

Project description:Chronic Lymphocytic Leukemia (CLL) cells multiply in secondary lymphoid tissue but the mechanisms leading to their proliferation are still uncertain. In addition to BCR-triggered signals, other microenvironmental factors might well be involved. In proliferation centres, leukemic B cells are in close contact with CD4+CD40L+Â T cells. Therefore, we here dissected the signals provided by autologous activated T cells (Tact) to CLL cells. Although the gene expression profile induced by Tact was highly similar to that induced by sole CD40 signaling, an obvious difference was that Tact induced proliferation of CLL cells. We determined that stimulation with only CD40L+IL-21 was sufficient to induce robust proliferation in CLL cells. We then defined an IL-21-induced gene signature in CLL, containing components of JAK-STAT and apoptosis pathways, and this signature could be detected in lymph node (LN) samples from patients. Finally, we could detect IL-21 RNA and protein in LN, and IL-21 productionÂ ex vivoÂ by LN CD4+CXCR5+ follicular helper T cells. These results indicate that, in addition to BCR signaling, activated T cells might contribute to CLL cell proliferation via CD40 and IL-21. Targeting these signaling pathways might offer new venues for treatment of CLL.Â CLL cells were cultured under different conditions for 16 hours and then sorted to purity as CD20+ CD5+ cells.

2013-10-07 | E-GEOD-50572 | biostudies-arrayexpress

Gene expression study in CLL of B-cell receptor triggering (miRNA study)

Project description:The B-cell receptor (BCR) plays an important role in pathogenesis and progression of chronic lymphocytic leukemia (CLL). We investigated the BCR triggering-dependent microRNA modulation by stimulating CLL cells with immobilized anti-IgM. miRome of immobilized anti-IgM stimulated CLL cells (n=16) identified a substantial upregulation of miR-132 in both unmutated (UM) and mutated (M) IGHV subgroups. A parallel gene expression profile and an in-silico analysis to identify miR-132 target genes¸ allowed us to focus on SIRT1, that encodes for a histone deacetylase targeting several proteins including TP53. We defined a reduction of SIRT1 protein levels upon immobilized anti-IgM stimulation (P=0.001), and a concomitant increase in TP53 acetylation (P=0.0072). The TP53 target gene CDKN1A was consistently up-regulated in immobilized anti-IgM stimulated CLL cells. Of note, the miR-132 constitutive expression levels in CLL cases (n=134) were of similar magnitude of those obtained in in vitro immobilized anti-IgM stimulated CLL cells. Additionally, high miR-132 expression levels retained a favorable prognostic impact in M (P=0.005), but not in UM CLL patients (P=0.968). The described miR-132/SIRT1/TP53 axis, sequentially characterized by BCR triggering, miR-132 up-regulation, SIRT1 down-regulation and TP53 acetylation, should be considered in the light of emerging drugs targeting the BCR pathway in CLL. investigated the BCR triggering-dependent gene expression modulation by stimulating CLL cells with immobilized anti-IgM.

2014-01-01 | E-GEOD-52775 | biostudies-arrayexpress

Selective Targeting of the Proliferating Compartment in Chronic Lymhocytic Leukemia by Inhibition or Downregulation of Aurora Kinases

Project description:Chronic lymphocytic leukemia (CLL) B-cells receive signals from the lymph node and bone marrow (BM) microenvironments that regulate their survival and proliferation. These signals and the pathways that propagate them to the interior of the cell represent potential targets for therapeutic intervention. To characterize the pathways that are activated by the BM microenvironment in CLL cells in vivo, we performed gene expression profiling of tumor cells purified from BM and peripheral blood. Functional classification analysis revealed that the most frequently upregulated genes in BM-CLL cells are genes involved in cell cycle and mitosis. Among the most significantly overexpressed were the Aurora A and B kinases. To investigate whether these kinases could represent potential therapeutic targets in CLL, we performed RNA interference experiments in the CLL cell lines MEC1 and EHEB. Downregulation of Aurora A and B inhibited the proliferation and induced apoptosis in these cells. Similar effects were observed with the pan-Aurora kinase inhibitor VX-680 in primary CLL cells induced to proliferate by CpG-ODN and IL-2. VX-680 also inhibited leukemia growth in vivo in a mouse model of CLL. These data suggest that inhibition of Aurora kinases could represent a potential strategy to selectively target the proliferating compartment in CLL. To identify gene expression related to microenvironmental stimuli in B-cell Chronic Lymphocytic Leukemia (CLL) cells in vivo, expression profiles of CLL cells purified (>95%) from bone marrow (BM) and peripheral blood (PB) were compared. Paired BM and PB samples from 6 individuals were used for this analysis.

2011-07-25 | E-GEOD-30896 | biostudies-arrayexpress

Expression data from activated NK cells [miRNA]

Project description:Natural Killer (NK) cells present natural cytotoxicity against tumor cells, although their activity is increased after activation.NK cell activation depends on a complex intracellular signaling process mediated by activating and inhibitory receptors and the functional outcome depends on the integration of the activating and inhibitory signals received. Soluble cytokines and/or ligands on target cells bind the NK cell receptors, and hence, influence the final NK cell response: attack versus ignorance. We used microarrays to detail the global programme of gene expression underlying NK cell activation by IL-2, a MHC-I-deficient target cell (K562)+IL-2 and an EBV-target cell (R69). PBLs from 4 different donors were activated by 100 U/ml IL-2; K562+IL-2 or R69 cells. After 5 days we obtained RNA and miRNA from naÃ¯ve NK cells or from NK cells activated with the above mentioned stimuli, with more than 90% of purity. The 16 RNA samples were used to generate cDNA libraries that were hybridized on Human Gene 1.1ST arrays (Affymetrix) and analyzed with the Affymetrix Gene Chip Command Console Software v3.0 (AGCC 3.0, AffymetrixÂ®) and the Expression Console Software v1.1 (AffymetrixÂ®).

2014-09-09 | E-GEOD-50839 | biostudies-arrayexpress

Defective Drosha Processing Contributes to Downregulation of MiR-15/-16 in Chronic Lymphocytic Leukemia.

Project description:MIR15A and MIR16-1, located in chromosomal band 13q14, are tumor suppressor miRNAs often deleted and downregulated in chronic lymphocytic leukemia (CLL). This downregulation is not only due to loss of 13q, as it occurs also in 13q+/+ CLL patients. We found that a subgroup of CLL patients has a dysregulation of miR-15 /-16 processing intermediates due to defective processing by Drosha. These patients have reduced levels of miR-15a, miR-16 and miR-15b (another member of the miR-15 family), but not of most other miRNAs. Thus, we show that modulation of miRNA maturation leads to specific downregulation of a family of tumor suppressor miRNAs in leukemic cells. 11 normal processing CLL sample; 12 processing defective CLL patients

2011-12-31 | E-GEOD-30927 | biostudies-arrayexpress

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2022-05-29 | E-MTAB-4899 | biostudies-arrayexpress

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