Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

MRNA-sequencing of 293T-no dice transfected with miR-16, miR-214, or KSHV-miR-K6-5p

ABSTRACT: The viral miRNA miR-K6-5p encoded by the DNA tumor virus Kaposi’s sarcoma-associated herpesvirus exhibits offset, sequence similarity with the tumor suppressive cellular miR-15/16 family, as well as sharing a short seed match to the cellular miR-214 (nts 2-7). We investigated how gene regulation by the viral miR-K6-5p is related to regulation by these cellular miRNAs by performing transcriptome analysis. mRNA-Seq was done in HEK 293T NoDice cells (Bogerd et al., RNA 2014) lacking Dicer which severely impaired the maturation of miRNAs thereby eliminating confounding effects of endogenously expressed miR-15/16 family. We transfected mature miRNA mimics of miR-16, miR-K6-5p wild-type, a variant of miR-K6-5p with a U at nt 1 instead of a C to control of RISC loading (miR-K6 5’U), miR-214, or a control mimic into NoDice cells, and harvested total RNA 2 days post-transfection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128576 | GEO | 2019/11/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

mRNA-sequencing of 293T-no dice transfected with miR-16, miR-214, or KSHV-miR-K6-5p

Project description:mRNA-sequencing of 293T-no dice transfected with miR-16, miR-214, or KSHV-miR-K6-5p

| PRJNA528188 | ENA

Low miR-214-5p expression correlates with aggressive subtypes of pediatric ALCL with non-common histology

Project description:The small RNA landscape of pediatric ALK-positive ALCL was defined by RNA sequencing. Overall, 121 miRNAs were significantly dysregulated in ALCL compared to non-neoplastic lymph nodes. The most up-regulated miRNA was miR-21-5p, while miR-19a-3p and miR-214-5p were reduced in ALCL. Characterization of miRNA expression in cases that relapsed after first line therapy disclosed a significant association between miR-214-5p down-regulation and aggressive non-common histology.

2021-05-12 | GSE171323 | GEO

Impact of miR-199-5p, miR-199a-3p and miR-214-3p overexpression on human lung fibroblasts

Project description:To identify putative novel specific targets of miR-199-5p, miR-199a-3p and miR-214-3p, we overexpressed these miRNAs in human MRC5 pulmonary fibroblasts (CCL-171) using synthetic pre-miRNAs or a synthetic “negative” pre-miRNA control (miR-Neg). RNA samples were harvested 48 hours post-transfection and 3 independent experiments were carried out.

2019-04-11 | GSE97824 | GEO

miR-1307-5p counteracts breast cancer angiogenesis and metastasis

Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.

2024-12-11 | PXD041087 | Pride

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

Identification of miR-16/29 targets in adipocytes by LC-MSMS

Project description:Cancer cachexia is a multifactorial metabolic syndrome defined by the rapid loss of skeletal muscle mass and the loss of fat mass. Up 80% of cancer patients at the late stage with cachexia suffer from progressive atrophy of adipose tissue. Unlike studies on skeletal muscle wasting, there is limited research on fat loss in cachexia. It was noted that most patients suffer from fat loss as cancer progress. Fat loss precedes muscle loss, is associated with shorter survival, and is variable to timing and intensity in various cancer populations. Increased lipolysis may be the leading cause of fat loss in cancer cachexia. miRNAs are a class of non-coding RNAs of 19~25 nucleotides that regulate gene silencing by interacting with the 3’ untranslated region (UTR) of target mRNA to cause mRNA degradation and translational repression. miRNAs play multifaceted roles in pancreatic cancer proliferation, survival, metastasis, and chemoresistance. Aberrant expression of miRNA in circulating exosomes may play potential roles in modulating fat loss in cancer cachexia. We identified 2 miRNAs, miR-16 and miR-29, which have 2-fold higher expression existed in at PDAC cells. To explore which genes in adipogenesis and lipolysis were directly affected by miR-16-5p or/and miR-29a-3p, we analyzed the targets which were down-regulated in both miR-16-5p and miR-29a-3p-transfected 3T3-L1 cells by mass analysis.

2024-06-13 | PXD037862 | Pride

Identification of miR-16/29 targets in adipocytes by LC-MSMS

2024-06-13 | PXD037998 | Pride

Gene expression profiling of MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors

Project description:We have employed whole genome microarray to identify changes in gene expression in MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors at 72 hours after transfection.

2020-05-31 | GSE148847 | GEO

Identification of distinct miRNAs associated with SARS-CoV-2 infection

Project description:MicroRNAs (miRNAs) have been shown to play important roles in the pathogenesis of viral infections, but little is known about the miRNA alternations associated with SARS-CoV-2 infection. Here, we performed high throughout sequencing to detect miRNAs in the plasma samples collected from 61 healthy controls, 16 asymptomatic individuals and 100 symptomatic COVID-19 patients. In total, we identified 2,336 known miRNAs and 361 novel miRNAs, including 75 differentially expressed miRNAs with p value<0.05 between various groups. We also found a number of miRNAs that were associated with various clinical presentations and viral persistence of COVID-19, such as hsa-miR-370-3p, hsa-miR-146a-3p, hsa-miR-885-5p, hsa-miR-214-3p and hsa-miR-10b-5p. Further analysis of the target genes, gene ontology and KEGG pathways revealed a panel of miRNAs that were linked to immune responses, viral infections, inflammation and apoptosis. Our findings may help understand the contribution of miRNAs to the pathogenesis of COVID-19 and identify potential biomarkers and molecular targets for the diagnosis and treatment of SARS-CoV-2 infection.

2022-05-05 | GSE166160 | GEO

T cell-derived miR-214 mediates perivascular fibrosis in hypertension

Project description:Despite increasing understanding of the prognostic importance of vascular stiffening linked to perivascular fibrosis in hypertension, the molecular and cellular regulation of this process is poorly understood. We aimed to study the functional role of microRNA-214 (miR-214) in the induction of perivascular fibrosis and endothelial dysfunction driving vascular stiffening. Out of 381 miRs screened in the perivascular tissues (PVAT) in response to angiotensin II (Ang II)-mediated hypertension, miR-214 showed the highest induction (8-fold, p<0.01). MiR-214 induction was pronounced in perivascular and circulating T cells, but not in PVAT adipocytes. Global deletion of miR-214-/- prevented Ang II-induced periaortic fibrosis Col1a1, Col3a1, Col5a1 and Tgfb1 expression, hydroxyproline accumulation and vascular stiffening, without difference in blood pressure. Mechanistic studies revealed that miR-214-/- mice were protected against endothelial dysfunction, oxidative stress and increased Nox2, all of which were induced by Ang II in WT mice. Ang II-induced recruitment of T cells into PVAT was abolished in miR-214-/- mice. Adoptive transfer of miR-214-/- T cells into RAG1-/- mice resulted in reduced perivascular fibrosis compared to the effect of WT T cells. Ang II induced hypertension caused significant change in the expression of 1380 T cell genes in WT, but only 51 in miR-214-/-. T cell activation, proliferation and chemotaxis pathways were differentially affected. miR-214-/- prevented Ang II-induction of pro-fibrotic T cell cytokines (IL-17, TNF, IL-9 and IFN) and chemokine receptors (CCR1, CCR2, CCR4, CCR5, CCR6 and CXCR3). This manifested in reduced in vitro and in vivo T cell chemotaxis resulting in attenuation of profibrotic perivascular inflammation. Translationally, we show that miR-214 is increased in plasma of hypertensive patients and is directly correlated to pulse wave velocity as a measure of vascular stiffness.

2020-02-29 | GSE143809 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data