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RNA-Seq analysis of the WEHI-231-derived stable cell lines WEHI-control and WEHI-miR-148a

ABSTRACT: miRNAs regulate the expression of its targets genes by promoting mRNA degradation and translational repression. The goal of this study is to perform RNA-Seq in control or miR-148a-expressing WEHI-231 cell lines for the identification of miR-148a target genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE75809 | GEO | 2016/02/22

SECONDARY ACCESSION(S): PRJNA305410

REPOSITORIES: GEO

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RNA-Seq analysis of the WEHI-231-derived stable cell lines WEHI-control and WEHI-miR-148a

Project description:miRNAs regulate the expression of its targets genes by promoting mRNA degradation and translational repression. The goal of this study is to perform RNA-Seq in control or miR-148a-expressing WEHI-231 cell lines for the identification of miR-148a target genes. WEHI-control and WEHI-miR-148a cells were stimulated with anti-IgM (2 ug/ml) for 14 h. Total RNA was extracted, enriched for polyA-containing RNAs and submitted to RNA-Seq.

2016-02-22 | E-GEOD-75809 | biostudies-arrayexpress

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Project description:Long-lived antibody-secreting plasma cells are essential to establish humoral memory against pathogens. While a plasma cell gene signature has been established, elaborate key regulators remain enigmatic.The plasma cell signature microRNA miR-148a favors in vitro differentiation of plasmablasts by repressing the germinal center transcription factor Bach2 and pro-apoptotic BIM and PTEN. To determine whether miR-148a fine-tunescontrols the in vivo development of B cells into long-lived plasma cells, we established mice with a genomic, conditional and inducible deletion of miR-148a. The analysis of miR-148a-deficient mice revealed reduced serum Ig, decreased numbers of newly formed plasmablasts and a reduced CD19-negative, CD93-positive long-lived plasma cells compartment. RNASeq and metabolic analysis showed an impaired glucose uptake and oxidative phosphorylation-based energy metabolism, altered abundance of homing receptors CXCR3 (increase) and CXCR4 (reduction) in miR-148a-deficient plasma cells. These findings establish the importance of miR-148a as a regulator of the differentiation and maintenance of late CD19-negative mature plasma cells by controlling their metabolism and retention in the bone marrow niche. clearly undermine our model of miR-148a as a regulator of the maintenance of long-lived plasma cells.

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Project description:Post-transcriptional regulation of genes is heavily dependent on the action of miRNAs. miRNAs take part in various cellular processes and have been shown to be crucial in oncogenesis. Identification of miRNA targets is crucial for understanding its functions in different cellular contexts. miR-148a-3p is highly expressed in HCT116 cells and several other cell lines. However, the studies about mRNA targetting activitiy of this miRNA was limited. In this study, we aimed at identifying target repotoire of miR-148a-3p by using HCT116 DROSHA-KO model. We found several genes that are under miR-148a-3p regulation, including several reported targets. We next found the negative association between miR-148a-3p and DDX6, one of the identified gene, in leukemia. We examined DDX6 functions in this cancer and showed that the depletion of DDX6 helps impair leukemia cell growth, promote apoptosis and increase survival rate of transplanted mice. We then identified that DDX6 functions to suppress TXNIP, a well known tumor suppressor in leukemia and various types of cancer. Our findings uncovered the regulation axis between miR-148a-3p/DDX6/TXNIP in leukemia which provides molecular mechanism basis for therapeutic treatment directions.

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Mus musculus

Project description:RNA-Seq analysis of the WEHI-231-derived stable cell lines WEHI-control and WEHI-miR-148a

| PRJNA305410 | ENA

Transcriptome analysis of WEHI B lymphoma cells overexpressing individual NFATc1 proteins

Project description:In lymphocytes, NFATc1 is the most prominent NFAT transcription factor which play a crucial role in the fate and activity of peripheral T and B cells. NFATc1 is synthesized in two prominent isoforms, the inducible short isoform NFATc1/aA and the constitutively expressed long isoform NFATc1/C. Several lines of evidence suggested that both isoforms differ markedly in their function. It was speculated that NFATc1/aA supports the proliferation and survival of lymphocytes, whereas NFATc1/C should support apoptosis and anergy induction. To proof this hypothesis we established WEHI 231 B lymphoma cells that stably (over-) express either NFATc1/aA or NFATc1/C. In preliminary experiments we could should that WEHI cells overexpressing NFATc1/aA were protected against apoptosis induction, while cells overexpressing NFATc1/C should a higher apoptosis rate. Transcriptom analysis of WEHI-231 cells overexpressing either NFATc1/aA or NFATc1/C were performed, along with a control group of WEHI-231 cells overexpressing the E.coli enzyme BirA Ligase (which is also present in all target cell lines since for further molecular assays the NFATc1 proteins were expressed as chimeric protein containing C-terminal bio-tags. The experimental results obtained indicate that the both NFATc1 proteins, NFATc1/aA and NFATc1/C, differ tremendously in their transcriptional properties.

2016-07-01 | E-MTAB-4665 | biostudies-arrayexpress

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