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Gene expression profiles of U87 cells after transfection with hsa-miR-145-5p and 31-5p

ABSTRACT: We analyzed the expression profiles of hsa-miR-145-5p or hsa-miR-31-5p-targeting genes relating to invasion or migration after co-overexpression of hsa-miR-145-5p and 31-5p

ORGANISM(S): Homo sapiens

PROVIDER: GSE83643 | GEO | 2016/06/23

SECONDARY ACCESSION(S): PRJNA326586

REPOSITORIES: GEO

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Gene expression profiles of U87 cells after transfection with hsa-miR-145-5p and 31-5p

Project description:We analyzed the expression profiles of hsa-miR-145-5p or hsa-miR-31-5p-targeting genes relating to invasion or migration after co-overexpression of hsa-miR-145-5p and 31-5p Gene expression profiles of U87 cells after co-transfection with hsa-miR-145-5p and 31-5p mimics, and U87 cells after transfection miR mimic negative control

2016-06-23 | E-GEOD-83643 | biostudies-arrayexpress

Hsa-miR-31-5p controls a metabolic switch in psoriatic keratinocytes that identifies therapeutic intervention

Project description:Next to genetic alterations, it is being recognized that the cellular environment also acts as a major determinant in onset and progression of disease. In cases where different cell types contribute to the final disease outcome, this imposes environmental challenges as different cell types likely differ in their extracellular dependencies. A number of skin diseases, including psoriasis is characterized by a combination of keratinocyte hyperproliferation and immune cell activation. Activation of immune cells involves increased glucose consumption thereby intrinsicly limiting glucose availability for other cell types. Thus, these type of skin diseases require metabolic adaptations that enable coexistence between hyperproliferative keratinocytes and activated immune cells in a nutrient-limited environment. Hsa-microRNA-31-5p (miR-31) is highly expressed in keratinocytes within the psoriatic skin. Here we show that miR-31 expression in keratinocytes is induced by limited glucose availability and enables increased survival of keratinocytes under limiting glucose conditions, by increasing glutamine metabolism. In addition, miR-31 induced glutamine metabolism results in secretion of specific metabolites (aspartate and glutamate) but also secretion of immuno-modulatory factors. We show that this miR-31-induced secretory phenotype is sufficient to induce Th17 cell differentiation, a hallmark of psoriasis. Inhibition of glutaminase (GLS) using CB-839 impedes miR31-induced metabolic rewiring and secretion of immuno-modulatory factors. Concordantly, pharmacological targeting of GLS alleviated psoriasis pathology in a mouse model of psoriasis. Together our data illustrate an emerging concept of metabolic interaction across cell compartments that characterizes disease development, which can be employed to design effective treatment options for disease, as shown here for psoriasis.

2023-02-06 | PXD029030 | Pride

Expression analysis of Hsa-miR-145-5p overexpressed laryngeal squamous carcinoma cell line TU177

Project description:Investigation of whole genome gene expression level changes in laryngeal squamous carcinoma cell line TU177 in response to overexpressed miR-145-5p. Differentially expressed protein-coding genes in the human laryngeal squamous carcinoma cells TU177 overexpressing miR-145-5p were identified by microarray analysis.

2017-12-31 | GSE92678 | GEO

PETACC-8 miR-31-3p and miR-31-5p Ancillary Study

Project description:This is a prospective-retrospective study to determine if the expression of the miRNA’s miR-31-3p and miR-31-5p are prognostic of patient outcomes or predictive of the benefit from anti-EGFR therapy in stage III Colon Cancer. The present study will utilize FFPE tumor samples collected from patients enrolled in the PETACC-8 study conducted by the Fédération Francophone de Cancérologie Digestive (FFCD). This phase 3 clinical trial prospectively randomized fully resected stage III colon cancer patients to receive adjuvant treatment with either FOLFOX-4 plus cetuximab or FLOFOX-4 alone.

| 2260465 | ecrin-mdr-crc

Sequencing of synthetic small RNAs hsa-miR-34b-5p, hsa-miR-449c-5p and their isomir variant

Project description:The aim of this small RNA Seq is to determine if the sequence reads observed for hsa-miR-34b-5p and hsa-miR-449c-5p represent library artifacts or sequencing artifacts

2017-06-12 | GSE77249 | GEO

Hsa-miR-139-5p expression regulates the abundance of proteins related to poor survival cancer in CAL-62 thyroid cancer cell line

Project description:We studied the impact of hsa-miR-139-5p on the protein output by means of an iTRAQ-based approach. First, we established two CAL-62 isogenic cell lines expressing either the mature hsa-miR-139-5p or a non-targeting control upon a doxycycline inducible promoter (PTRE3G-tGFP, Dharmacon). Total proteins of P-tGFP-hsa-miR139-5p untreated or treated with doxycycline (1ug/ml) for 96 and 120 hours were isolated and labeled with iTRAQ® reagent 8-plex. Two independent experiments were performed.

2019-08-13 | PXD011901 | Pride

Hsa-miR-371a-5p and hsa-miR-518a-3p regulated genes in choriocarcinoma cells

Project description:We report the application of transcriptome sequencing for investigating of the hsa-miR-371a-5p and hsa-miR-518a-3p regulated genes. JAR, JEG-3 and BeWo choriocarcinoma cells were transfected with hsa-miR-371a-5p or hsa-miR-518a-3p inhibitors or control inhibitors. Totally, 237, 132 and 277 genes with > 2 folds change and adjusted P < 0.05 were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-371a-5p knockdown. Meanwhile, 229, 269 and 191 genes were upregulated in JAR, JEG-3 and BeWo cells respectively after hsa-miR-518a-3p knockdown. The top upregulated genes included many oncogenes or oncogenesis associated ones. Enrichment analysis showed hsa-miR-371a-5p and hsa-miR-518a-3p regulated diverse pathways related to tumorigenesis and metastasis. Our results would be helpful for the searching of early molecular biomarkers and therapeutic targets for gestational trophoblastic neoplasia.

2018-11-01 | GSE106394 | GEO

A Seed Sequence Variant in miR-145-5p causes Multisystem Smooth Muscle Dysfunction Syndrome (MSMDS)

Project description:Multisystem smooth muscle dysfunction syndrome (MSMDS) is a smooth muscle myopathy with major dysfunction in multiple organ systems. Described cases have been exclusively associated with recurrent missense variants at amino acid position 179 in the ACTA2 gene. We describe a patient with multiple major manifestations of MSMDS including steno-occlusive cerebrovascular arteriopathy, prune belly syndrome, gastrointestinal dysmotility, bladder dysfunction, and pupillary hyporeactivity without variation in ACTA2. Whole genome sequencing revealed a single nucleotide variant contained within the seed sequence of MIR145, which encodes the smooth muscle associated microRNA; hsa-miR-145-5p. RNA expression analysis on patient-derived fibroblasts was consistent with actin cytoskeletal dysfunction, and mutant miR-145-5p was unable to mediate cytoskeletal modulation of smooth muscle cells. MSMDS can be caused by a loss-of-function mutation in the smooth muscle differentiation factor, miR-145-5p, the first described non-coding genetic vasculopathy.

2023-12-14 | GSE220038 | GEO

Exosomal miR-145-5p derived from plasma of ARDS promotes apoptosis of renal tubule epithelial cells by JNK signal pathway

Project description:This experiment is designed to investigate the impact of exosomal miR-145-5p on the functional pathway and molecules on RPTEC cells. Data-independent acquisition (DIA) proteomics was conducted in the RPTEC cells transfected with miR-145-5p mimic or scramble control.

2023-03-28 | PXD041158 | iProX

Hsa-miR-500a-5p target discovery

Project description:Hsa-miR-500a-5p (miR500a) activity has been associated with breast cancer survival. We used gene expression arrays (Illumina HumanHT-12 V4.0) to discover relevant targets of miR500a.

2017-11-27 | GSE92564 | GEO

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