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Transcriptional profile comparing Hep3B transfected with miR-19b inhibitor with Hep3B transfected with control

ABSTRACT: miR-19b was up-regulated with hepatocellular carcinoma. We compared the transcriptional profile of Hep 3B transfected with miR-19b inhibitor with Hep3B transfected with control to identify genes affected by miR-19b knockdown. Hep 3B_miR-19b transfected vs Hep 3B_control transfected

ORGANISM(S): Homo sapiens

SUBMITTER: Chung-Lin Hung

PROVIDER: E-GEOD-69519 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional profile comparing Hep3B transfected with miR-19b inhibitor with Hep3B transfected with control

Project description:miR-19b was up-regulated with hepatocellular carcinoma. We compared the transcriptional profile of Hep 3B transfected with miR-19b inhibitor with Hep3B transfected with control to identify genes affected by miR-19b knockdown.

2015-07-22 | GSE69519 | GEO

A global transcriptome analysis of human epidermal keratinocytes upon overexpression of microRNA-19a or microRNA-19b or microRNA-20a

Project description:Several members from microRNA 17-92 cluster, i.e. miR-19a, miR-19b and miR-20a, were found up-regulated in human epidermal keratinocytes at wound-edges compared to the intact skin; however their biological role in keratinocytes during wound repair has not been studied. To study the genes regulated by miR-19a, miR-19b and miR-20a, we transfected miRNA specific mimics, i.e. pre-miR-19a, pre-miR-19b or pre-miR-20a into human primary epidermal keratinocytes to overexpress them. We performed a global transcriptome analysis of keratinocytes upon overexpression of miR-19a or miR-19b or miR-20a using Affymetrix arrays.

2017-02-15 | GSE93110 | GEO

miR-17-92 sustains lymphoma growth by fine-tuning MYC

Project description:The synergism between c-MYC and miR-17-19b, a truncated version of the miR-17-92 cluster, is well documented during tumor initiation. However, little is known about miR-17-19b function in established cancers. Here we investigate the role of miR-17-19b in c-MYC-driven lymphomas by integrating SILAC-based quantitative proteomics, transcriptomics and 3’ UTR analysis upon miR-17-19b overexpression. We identify over one hundred novel miR-17-19b targets, of which 40% are co-regulated by c-MYC. Down-regulation of a new miR-17/20 target Chek2 increases the recruitment of HuR to c-MYC transcripts, resulting in the inhibition of c-MYC translation and thus interfering with in vivo tumor growth. Hence, in established lymphomas, miR-17-19b fine-tunes c-MYC activity through a tight control of its function and expression, ultimately ensuring cancer cell homeostasis. Our data highlight the plasticity of miRNA function, reflecting changes in the mRNA landscape and 3’ UTR shortening at different stages of tumorigenesis.

2015-11-06 | PXD002810 | Pride

Differential miRNA expression profiles betweenHBV-related HCC tumor versus non-tumor liver tissue

Project description:miRNA played an important role in the process of carcinogenesis in HBV related hepatocellular carcinoma. Therefore, we performed miRNA microarray to evaluate the miRNAs that expressed differentially between HCC tumor versus non-tumor liver tissues. RNA was extracted from snap fresh tissue collected from resected HCC tumor and adjacent non-tumor liver tissues. All HCC tumors were HBV-associated HCC.

2015-07-22 | E-GEOD-69580 | biostudies-arrayexpress

Wildtype, miR-1-1 KO, miR-1 Double het P2 mixed strain heart analysis (MoGene 2.0 ST Arrays).

Project description:Neonatal hearts (P2) from wildtype, miR-1-1 null and miR-1-2 +/-: miR-1-1 +/- double heterozygote animals were isolated and total RNA was extracted with TRIzol (Invitrogen), following the manufacturer’s suggested protocol. Genomic DNA was removed using a gDNA eliminator column (Qiagen). Samples were hybridized to Affymetrix mouse genechip ST 2.0 arrays. Mouse strain for all samples is: Mixed 129 x C57BL/6 Three groups: miR-1-1, miR-1 double het, wildtype, all compared against each other. Samples are all from neonatal hearts.

2013-10-19 | E-GEOD-51394 | biostudies-arrayexpress

Homo sapiens

Project description:Transcriptional profile comparing Hep3B transfected with miR-19b inhibitor with Hep3B transfected with control

| PRJNA285784 | ENA

microRNA profiling of multiple myeloma bone marrow

Project description:Bone marrow microenvironment in MM contains a unique miR signature, which is partially present and detectable in the peripheral blood. A subset of miRs (let-7i, miR-106b, miR-15a, and miR16) shows aberrant expression in the precursor lesion of MGUS, while aberrant expression of other miRs (let-7a, miR-15a/b, miR-19b, miR-20a, miR-21, miR-223, and miR-361) is associated with cell proliferation and disease progression. miRNA profiling was performed using Agilent miRNA array platforms with RNAs isolated from the bone marrow supernatant of multiple myeloma.

2016-07-01 | E-GEOD-49261 | biostudies-arrayexpress

MicroRNA-19b exacerbates systemic sclerosis through promoting Th9 cells

Project description:Systemic sclerosis (SSc) is a chronic autoimmune disease characterized with fibrosis of skin and multiple vital organs, but the immunological pathogenesis of SSc remains largely unknown. We show here that microRNA-19b (miR-19b) promotes IL-9-producing CD4+ T cells (Th9) that exacerbate SSc. Specifically, TGF-b plus IL-4 induced expression of TNF receptor associated factor 6 (TRAF6) through phosphorylated Smad3 linker region site Serine 213 (p-Smad3L-Ser213) and activated it through K63 ubiquitination by suppressing the leucine-rich-repeat-containing protein 3 (NLRC3). TRAF6 consequently formed complex with and activated TGF-b activated kinase 1 (TAK1). TAK1 promoted nuclear factor kappa B (NFκB) p65 activation, which then specifically upregulated miR-19b. miR-19b activated Il9 gene expression and promoted Th9 differentiation by directly targeting and suppressing atypical E2F family member E2f8 gene, a repressor for Il9 gene transcription. Importantly, Th9 cells played a critical role in the development and pathogenesis of experimental SSc by promoting the fibrosis in mice induced with Bleomycin. miR-19b and IL-9 were increased in CD4+ T cells in experimental SSc in mice and also in patients with SSc. Strikingly, inhibition of miR-19b resulted in fewer Th9 cells and attenuated fibrotic manifestations and ameliorated the disease in SSc mice. Our study identifies miR-19b as a key factor of Th9 cells that are involved in the pathogenesis of SSc. Our findings should have clinical implications for patients with SSc.

2024-08-21 | GSE269954 | GEO

5b763f6e-2031-4d46-913d-ee7491e7e50c - samples

Project description:iPSC-derived neurons were treated with mimics and inhibitors of the miRNAs miR-150-5p, hsa-mir-193a-3p and hsa-miR-19b-3p. RNA-sequencing was then performed to examine the effects of miRNA up-regulation and inhibition.

| EGAD00001006844 | EGA

miRNA expression in moncytes in response to estradiol

Project description:This profiling experiment evaluates the global changes in miRNA expression in monocytic cells in response to 10 nM Estradiol treatment. Levels of circulating 17β-estradiol (E2) may influence the progression of many human diseases. We hypothesize that E2 modulates the inflammatory response of circulating innate immune cells through microRNA (miRNA)-based modulation of secretory leucoprotease inhibitor (SLPI), a multifunctional antiprotease with immunomodulatory functions. Monocytes were treated with E2 or control, and differentially expressed miRNAs in monocytes were identified using PCR profiling. Cells were transfected with miRNA mimics or antimiRs and SLPI mRNA and protein levels were quantified by qPCR and ELISA, respectively. Luciferase activity assay was performed using SLPI-3’UTR reporter constructs. ChIP was carried out on monocytes treated with E2. SLPI expression is downregulated, and miR-19 is upregulated in response to E2 in monocytes, via increased MIR17HG promoter activity mediated by c-MYC. Transfection of monocytic cells with premiR-19b reduced SLPI expression. This was abrogated using antimiRs against miR-19b. miR-19b directly binds the SLPI 3’UTR as determined by luciferase activity assay. The data show that E2 decreases expression of SLPI in human monocytic cells, via changes in miRNA expression and further highlights the potential for E2 to modulate key components of innate immunity. Modulation of these miRNAs may offer a new therapeutic approach in the treatment of chronic inflammatory diseases.

2016-07-12 | GSE84254 | GEO

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