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Gene Expression in 70Z/3 pre-B cells Stably Overexpressing Individual members of the mirn23a MiRNA Cluster

ABSTRACT: Expression of the mirn23a cluster in murine hematopoietic progenitors blocks B cell development. Overexpressed individual cluster members miRs-23a, 24-2, and -27a in 70/3 mouse pre-B cells in order to examine changes in gene expression that would potentially reveal targets of the miRs relevant to hematopoiesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE65874 | GEO | 2015/02/12

SECONDARY ACCESSION(S): PRJNA275257

REPOSITORIES: GEO

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Gene Expression in 70Z/3 pre-B cells Stably Overexpressing Individual members of the mirn23a MiRNA Cluster

Project description:Expression of the mirn23a cluster in murine hematopoietic progenitors blocks B cell development. Overexpressed individual cluster members miRs-23a, 24-2, and -27a in 70/3 mouse pre-B cells in order to examine changes in gene expression that would potentially reveal targets of the miRs relevant to hematopoiesis. Two independent 70Z/3 cell lines for each experimental group were generated (MSCV, miR-23a, miR-24-2, and miR-27a). RNA was generated and hybridized on Affymetrix microarrays.

2015-02-12 | E-GEOD-65874 | biostudies-arrayexpress

Integrating CRISPR knockout, interference, and activation to dissect the functional role and underlying signaling of microRNA-23a-27a-24-2 cluster in hepatocellular carcinoma

Project description:The miR-23a-27a-24-2 cluster is overexpressed in human cancers, including hepatocellular carcinoma (HCC). However, the role of three mature miRNAs of the miR-23a-27a-24-2 cluster in HCC is still controversial. Also, the integrative role of the miR-23a-27a-24-2 cluster in HCC remains elusive. In the present study, using CRISPR knockout (KO), CRISPR interference (CRISPRi), and CRISPR activation (CRISPRa) technologies, we established an endogenous miR-23a-27a-24-2 controllable and various knockout (KO) cell models, which were used to dissect the functional role and underlying signaling of the miR-23a-27a-24-2 cluster. Either miR-23a KO or miR-27a KO reduced cell growth in vitro and in vivo. Of particular note, endogenous miRNAs in the miR-23a-27a-24-2 cluster were effectively regulated by CRISPRi/a, identifying an integrated oncogenic role of the miR-23a-27a-24-2 cluster in HCC cells. Functional analysis showed that miR-23a KO and miR-27a KO led the cell cycle arrest, especially at the G2/M phase, by reducing CDK1/cyclin B activation in HCC cells. Furthermore, a high-throughput RNA-seq approach with miRNA target prediction identified the miR-23a/miR-27a-regulated gene network, further validated by various technologies. In addition, miR-23a and miR-27a have opposite roles in cell migration and mesenchymal-epithelial transition. However, an integrated analysis by CRISPRi/a suggested an oncogenic role of the miR-23a-27a-24-2 cluster in cell migration, which may require a miR-23a-BMPR2-Smad-Snail axis in HCC cells. Thus, our CRISPRi/a study offers a valuable research tool for dissecting the integrated role and underlying mechanism of an endogenous miRNA cluster. Also, this CRISPR approach may provide new routes of miRNA intervention for miRNA targeted therapy.

2024-09-30 | GSE199332 | GEO

Differential expression of genes after over expression of miR-23a~27a~24-2 cluster in human embryonic kidney cells

2010-07-02 | GSE20158 | GEO

Differential expression of genes after over expression of miR-23a~27a~24-2 cluster in human embryonic kidney cells

Project description:The experiment was deigned to identify the genes which get altered after the over expression of miR-23a~27a~24-2 cluster in HEK293T cells. The HEK293T cells plated in 6-well plate were transfected with two different concentrations of cloned miRNA cluster i.e 2micrograms and 4micrograms per well. Biological duplicates of 3 samples were used viz. control HEK293T cells, HEK293T cells transfected with 2micrograms of the cloned cluster and HEK293T cells transfected with 4micrograms of the cloned cluster.

2010-07-30 | E-GEOD-20158 | biostudies-arrayexpress

The miR-23a~27a~24-2 microRNA cluster promotes inflammatory polarization of macrophages

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MiRNA expression variation in primary NK cells treated with TGF-β1

Project description:Human NK cells activity against cancer cells is deeply suppressed by TGF-β1, an immunomodulatory cytokine that is released and activated in the tumor microenvironment. Moreover, our previous data showed that TGF-β1 modifies the chemokine receptor repertoire of NK cells. In particular, it decreases the expression of CX3CR1 that drives these effectors toward peripheral tissues, including tumor sites. In order to identify possible mechanisms mediating chemokine receptors modulation, we analyzed the miRNA profile of TGF-β1-treated primary NK cells. The analysis pointed out miR-27a-5p as a possible modulator of CX3CR1. We demonstrated the functional interaction of miR-27a-5p with the 3’ untranslated region (3’UTR) of CX3CR1 mRNA by two different experimental approaches: by the use of a luciferase assay based on a reporter construct containing the CX3CR1 3’UTR and by transfection of primary NK cells with a miR-27a-5p inhibitor. We also showed that the TGF-β1-mediated increase of miR-27a-5p expression is a consequence of miR-23a-27a-24-2 cluster induction. Moreover, we demonstrated that miR-27a-5p down-regulates the surface expression of CX3CR1. Finally we showed that Neuroblastoma cells induced in resting NK cells a downregulation of the CX3CR1 expression that was paralleled by a significant increase of miR-27a-5p expression. Therefore, the present study highlights miR-27a-5p as a pivotal TGF-β1-induced regulator of CX3CR1 expression.

2017-05-11 | GSE98769 | GEO

Mouse Articular chondrocyte LC-MSMS of wild-type, miR-26a -/- and cartilage-specific miR-23ab clusters knockout mice

Project description:To reveal the potential regulation target genes of miR-26a and miR-23a/b clusters in articular chondrocytes, we performed a multi-omics analysis of LC-MSMS and RNA-seq using cultured chondrocytes samples, which were primarily isolated from 3-week-old wild-type, miR-26a -/- (with or without miR-26a mimic transfection afterwards) or miR-23a/b cluster flox/flox;Col2a1-cre mice. For LC-MSMS, protein from TRIZOL reagent was extracted, nanoLC-MSMS was performed. An expression list was made to further explore the regulation targets of miR-26a and miR-23a/b clusters.

2023-01-25 | PXD031868 | Pride

iGAS cluster

Project description:iGAS cluster

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Integrating CRISPR knockout, interference, and activation to dissect the functional role and underlying signaling of microRNA-23a-27a-24-2 cluster in hepatocellular carcinoma

Project description:Integrating CRISPR knockout, interference, and activation to dissect the functional role and underlying signaling of microRNA-23a-27a-24-2 cluster in hepatocellular carcinoma

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Maize gene expression during infection with the Ustilago maydis mutant for cluster 19A and subdeletions for individual genes of cluster 19A

Project description:Many of the genes coding for secreted protein effectors are arranged in gene clusters in the genome of the biotrophic plant pathogen Ustilago maydis. The largest of these gene clusters, cluster 19A, encodes 24 secreted effectors. Deletion of the entire cluster results in severe attenuation of virulence. The generation and analysis strains carrying sub-deletions identified 9 genes significantly contributing to tumor formation after seedling infection. As the individual contributions of these genes to tumor formation were small, we studied the response of maize plants to the whole cluster mutant as well as to several individual mutants by array analysis. This revealed distinct plant responses, demonstrating that the respective effectors have discrete plant targets. Many of the genes coding for secreted protein effectors are arranged in gene clusters in the genome of the biotrophic plant pathogen Ustilago maydis. The largest of these gene clusters, cluster 19A, encodes 24 secreted effectors. Deletion of the entire cluster results in severe attenuation of virulence. The generation and analysis strains carrying sub-deletions identified 9 genes significantly contributing to tumor formation after seedling infection. As the individual contributions of these genes to tumor formation were small, we studied the response of maize plants to the whole cluster mutant as well as to several individual mutants by array analysis. This revealed distinct plant responses, demonstrating that the respective effectors have discrete plant targets. We used the Affymetrix maize genome array to analyze the transcriptional responses of maize to cluster 19A mutants and individual sub-deletions for the cluster 19A genes tin1, tin3, tin4 and tin5. We found plant responses to the mutants were significantly different although the macroscopic phenotypes of the individual mutants were very similar.

2014-09-01 | GSE48406 | GEO

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