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MiR-34a targets PDGFRA in proneural malignant glioma

ABSTRACT: To identify potential targets of miR-34a, we performed transcriptional profiling on proneural TS543 GBM cells, focusing on mRNAs whose levels decreased in response to miR-34a transfection as compared to control oligonucleotide. Proneural TS543 GBM cells were transfected with 100 nM hsa-miR-34a or control oligonucleotide using Hiperfect transfection reagent (Qiagen). After 3 days, RNA was isolated and expression analyses were performed using Illumina HT-12 bead array. The microarray dataset was normalized using a variance stable normalization (VSN) procedure in the ‘lumi’ package from the Bioconductor framework.

ORGANISM(S): Homo sapiens

SUBMITTER: Joachim Silber

PROVIDER: E-GEOD-34242 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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miR-34a targets PDGFRA in proneural malignant glioma

Project description:To identify potential targets of miR-34a, we performed transcriptional profiling on proneural TS543 GBM cells, focusing on mRNAs whose levels decreased in response to miR-34a transfection as compared to control oligonucleotide.

2012-03-27 | GSE34242 | GEO

Inferring transcriptional and microRNA-mediated regulatory programs in glioblastoma

Project description:Large-scale cancer genomics projects are profiling hundreds of tumors at multiple molecular layers, including copy number, mRNA and miRNA expression, but the mechanistic relationships between these layers are often excluded from computational models. We developed a supervised learning framework for integrating molecular profiles with regulatory sequence information to reveal regulatory programs in cancer, including miRNA-mediated regulation. We applied our approach to 320 glioblastoma profiles and identified key miRNAs and transcription factors as common or subtype-specific drivers of expression changes. We confirmed that predicted gene expression signatures for proneural subtype regulators were consistent with in vivo expression changes in a PDGF-driven mouse model. We tested two predicted proneural drivers, miR-124 and miR-132, both underexpressed in proneural tumors, by overexpression in neurospheres and observed a partial reversal of corresponding tumor expression changes. Computationally dissecting the role of miRNAs in cancer may ultimately lead to small RNA therapeutics tailored to subtype or individual. miRNA mimetics were transfected to PDGFRA amplified neurosphere cell lines. Gene expression was measured 24 hours after transfection

2011-10-11 | E-GEOD-32876 | biostudies-arrayexpress

Genome-wide analysis of the effect of supressing miR-34a on urothelial cells

Project description:MiR-34a appears to be protective against cancer. Blocking miR-34a results in pro-tumorigenic phenotypic changes. The purpose of this experiment was to identify gene expression changes that could potentially explain the pro-tumorigenic effects of anti-miR 34a transfection.

2017-07-05 | GSE59182 | GEO

MiRNA and lung cancer (INCA Project) - 16 RNG25k microarrays

Project description:To identify putative novel specific targets of mir-210, we overexpressed miR-210 as well as miR-34a and a siRNA targeted against E2F3 in A549 human adenocarcinoma cells by transfecting them with synthetic pre-miRNAs or a synthetic “negative” pre-miRNA as control (miR-Neg). RNA samples were harvested at 48 hours post-transfection and 2 independent experiments were carried out. 48 hours post-transfection, 2 independent experiments performed in dye-swap: miR-210 versus miR-Neg ; miR-34a versus miR-Neg ; si-E2F3 versus miR-Neg ; si-control versus miR-Neg.

2010-09-30 | E-GEOD-18695 | biostudies-arrayexpress

Homo sapiens

Project description:miR-34a targets PDGFRA in proneural malignant glioma

| PRJNA149773 | ENA

Gene expression profiling of miR-regulated genes in proliferating C2C12

Project description:We used microarrays to detail the global programme of gene expression upon the over-expression of seven different differentiation-associated, E1A-regulated microRNAs. seven different microRNAs (miR-1, miR-34a, miR-22, miR-365, miR-29a, miR-145 and Let-7b) and a negative control (AllStar, Qiagen) were over-expressed at 50nM for 36hrs in proliferating myoblasts. Three independent biological experiments were performed.

2012-09-01 | E-GEOD-26764 | biostudies-arrayexpress

Identification of SART3 as a pre-miR-34a–binding protein

Project description:MicroRNAs (miRNAs or miRs) are small, noncoding RNAs that are implicated in the regulation of nearly all biological processes. Global miRNA biogenesis is altered in many cancers and RNA-binding proteins (RBPs) have been shown to play a role in this process, presenting a promising avenue for targeting miRNA dysregulation in disease. miR-34a exhibits tumor-suppressive functions by targeting cell cycle regulators CDK4/6 and anti-apoptotic factor Bcl-2, among other regulatory pathways such as Wnt, TGF-, and Notch signaling. Many cancers show downregulation or loss of miR-34a, and synthetic miR-34a supplementation has been shown to inhibit tumor growth in vivo; however, the post-transcriptional mechanisms by which miR-34a is lost in cancer are not entirely understood. Here, we have used a proteomics-mediated approach to identify Squamous cell carcinoma antigen recognized by T-cells 3 (SART3) as a putative pre-miR-34a-binding protein. SART3 is a spliceosome recycling factor and nuclear RBP with no previously reported role in miRNA regulation. We demonstrate that SART3 binds pre-miR-34a with specificity over pre-let-7d and begin to elucidate a new functional role for this protein in non-small lung cancer cells. Overexpression of SART3 led to increased miR-34a levels, downregulation of the miR-34a target genes CDK4 and CDK6, and cell cycle arrest in the G1 phase. In vitro binding studies showed that the RNA-recognition motifs within the SART3 sequence are responsible for selective pre-miR-34a binding. Collectively, our results present evidence for an influential role of SART3 in miR-34a biogenesis and cell cycle progression.

2019-10-14 | PXD015278 | Pride

Gene expression profile in JAR (HTB-144, ATCC) cells with scrambled control or miR-34a mimic transfection

Project description:We examined gene expression variations in JAR cells between scrambled control and miR-34a mimic transfection

2024-10-17 | GSE279257 | GEO

Alteration of miRNome by recombinant ncRNA agents

Project description:Purpose: Identify whether recombinant ncRNAs are recognized by mammalian cells and processed into mature microRNAs, thus leading to the alteration of downstream target genes. In addition, we also explored whether cleavage is Dicer dependent. Methods: HEK293T (Dicer-WT) and 424 (Dicer-KO) cell lines were treated with 20nM of control tRNA (MSA), nCAR/miR-34a-5p, or nCAR/miR-34a-3p in triplicate. Results: Read counts of known miRNAs were analyzed using a miRDeep module, and read counts derived from nCAR/miR-34a-5p or nCAR/miR-124a-3p transfection were obtained by mapping sequence reads by an in-house developed PERL script. EdgeR was used to analyze significant (P-value < 0.05 and log2CPM > 6) differentially expressed miRNAs and sRNAs. Conclusions: Upon transfection of recombinant RNA agents in mammalian cells, nCAR/miR-34a-5p became the most dominant miRNA and was processed in a Dicer dependent manner, while nCAR/miR-124a-3p become the 7th most abundant miRNA and displayed comparable levels with or without Dicer. In both cases, different isoforms of the mature miRNA sequence were generated.

2020-09-01 | GSE103349 | GEO

Gene expression changes due to influenza virus induced miRNAs

Project description:The goal of this experiment was to determine gene expression changes during influenza A virus infection as the result of expression influenza virus inducible miRNAs in A549 cells. The gene expression profiling experiment was performed with 4 groups (mock infected, influenza A virus infected, influenza A virus infected in the presence of exogenous miR-141, miR-374b, miR-449b, miR-518b, and miR-1263, and influenza A virus infected in the presence of exogenous miR-147b, miR-190b, miR-199a, miR-512-5p, and miR-874 with 3 biological replicates for each group. Total RNA was purified from A549 cells that were mock infected or infected with influenza A virus (A/WSN/33, 5pfu/cell) alone or in the presence of miRNA mimics 10 hours after treatment.

2013-09-15 | E-GEOD-47937 | biostudies-arrayexpress

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