Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genes downregulated by miR-92a-1-5p overexpression in K562 cells treated with imatinib.

ABSTRACT: In order to indetify new target genes of miR-92a-1-5p in chronic myeloid leukemia, K562 cells carrying the BCR::ABL1 fusion gene were transiently transfected with miR-92a mimic or scramble and treated with imatinib. RNA was sequenced to identify genes expressed under imatinib treatment and downregulated after miR-92a-1-5p overexpression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE278906 | GEO | 2024/10/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profile of K562 treated with the combination of imatinib and miR-342-5P

Project description:To determine the specific gene expression of imatinib in CML cells with or without miR-342-5P expression, gene array analysis was performed.

2021-10-13 | GSE171659 | GEO

U937 scramble (Usc) vs U937 miR-194-5p (UmiR-194-5p)

Project description:Transcriptional profiling of U937 scramble vs U937 miR-194-5p (UmiR-194-5p)

2017-05-22 | GSE73646 | 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 |

Effect of Imatinib on chronic myelogenous leukemia

Project description:The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which is present in almost every patient with chronic myeloid leukemia. In this study, the tyrosine kinase inhibitor Imatinib was used for pharmacological inhibition of BCR-ABL1. Gene expression profiles of CML cell lines were analyzed in response to Imatinib treatment.

2010-10-10 | GSE24493 | GEO

Effect of imatinib on philadelphia chromosome positive acute lymphoblastic leukemia

Project description:The Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. In this study, the tyrosine kinase inhibitor imatinib was used for pharmacological inhibition of BCR-ABL1. Gene expression profiles of Ph+ ALL cell lines were analyzed in response to imatinib treatment.

2010-09-10 | GSE23743 | GEO

A Prospective Study of Colorectal Cancer Risk Population Screening Using Stool-based miR-92a Assay

Project description:Interventions: Screening Group:NA Primary outcome(s): miR-92a;hemoglobin Study Design: Diagnostic test for accuracy

| 81565 | ecrin-mdr-crc

The miR-92a–Cpeb3 axis safeguards neuronal function during neuroinflammation

Project description:Neuroinflammation causes neuronal injury in multiple sclerosis (MS) and other neurological diseases. MicroRNAs (miRNAs) are central modulators of cellular stress responses, but knowledge about miRNA–mRNA interactions that determine neuronal outcome during inflammation is limited. Here, we combined unbiased neuron-specific miRNA with mRNA sequencing to assemble the regulatory network that mediates robustness against neuroinflammation. As a critical miRNA-network hub we defined miR-92a. Genetic deletion of miR-92a exacerbated the disease course of mice undergoing experimental autoimmune encephalomyelitis (EAE), whereas miR-92a overexpression protected neurons against excitotoxicity. As a key miR-92a target transcript, we identified cytoplasmic polyadenylation element-binding protein 3 (Cpeb3) that was suppressed in inflamed neurons in mouse EAE and human MS. Accordingly, Cpeb3 deletion improved neuronal resistance to excitotoxicity and ameliorated EAE. Together, we discovered that the miR-92a–Cpeb3 axis confers neuronal robustness against inflammation and serves as potential target for neuroprotective therapies.

2023-11-06 | GSE220950 | GEO

miR-671-5p promotes epithelial-to-mesenchymal transition by downregulating FOXM1 expression in breast cancer

Project description:microRNA (miRNA) dysfunction is associated with a variety of human diseases including cancer. Our previous study showed that miR-671-5p was deregulated during breast cancer progression. We aim to decipher the functional mechanism of miR- 671-5p in breast cancer. We used microarrays to detail the global programme of gene expression after overexpression miR-671-5p in several breast cancer cell lines, and those altered genes might potentially under regulation of miR-671-5p contibuting to breast cancer developemtn. miR-671-5p or scramble control nucleotide were tranfected into breast cancer cell lines, including MCF7, MDA231 and SKBR3. Total RNA were extracted and hybridized on Affymetrix microarrays. We sought to identify the potential downstream target genes that under miR-671-5p regulation by overexpress miR-671-5p. Potential targets were predicted to see if it has binding sites matching miR-671-5p sequence by miRNA target prediction softwares.

2014-10-16 | E-GEOD-62411 | biostudies-arrayexpress

Effect of imatinib on philadelphia chromosome positive acute lymphoblastic leukemia

2010-09-10 | E-GEOD-23743 | biostudies-arrayexpress

Exosomal miR-92a-3p as a diagnostic biomarker for adenomyosis and its pathological mechanism

Project description:This study aimed to elucidate the role of microRNA miR-92a-3p in the pathogenesis of adenomyosis. We focused on understanding how miR-92a-3p in exosomes derived from ectopic lesions influences the behavior of endometrial cells, DRG neurons, and Human Umbilical Vein Endothelial Cells (HUVECs), and its potential as a non-invasive diagnostic biomarker. Our findings revealed that MiR-92a-3p is significantly upregulated in exosomes derived from ectopic lesions of adenomyosis. This upregulation was associated with enhanced migration and invasion capabilities in eutopic endometrial cells, DRG neurons, and HUVECs. Furthermore, the study demonstrated a significant correlation between the levels of MiR-92a-3p in urinary exosomes and the clinical symptoms of adenomyosis, suggesting its potential as a non-invasive biomarker for the disease. This study elucidates an exosomal signaling process via miR-92a-3p that drives pathological infiltration and angiogenesis to promote adenomyosis progression. Upregulated miR-92a-3p in biofluid exosomes shows promising non-invasive biomarker potential for diagnosis and monitoring of this disease. Our findings unveil novel targets and tools for improved clinical management.

2024-04-01 | GSE262302 | 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