Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Differential expression of genes after over expression of miR-23a~27a~24-2 cluster in human embryonic kidney cells

ABSTRACT: The experiment was deigned to identify the genes which get altered after the over expression of miR-23a~27a~24-2 cluster in HEK293T cells. The HEK293T cells plated in 6-well plate were transfected with two different concentrations of cloned miRNA cluster i.e 2micrograms and 4micrograms per well.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20158 | GEO | 2010/07/02

SECONDARY ACCESSION(S): PRJNA125619

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Differential expression of genes after over expression of miR-23a~27a~24-2 cluster in human embryonic kidney cells

Project description:The experiment was deigned to identify the genes which get altered after the over expression of miR-23a~27a~24-2 cluster in HEK293T cells. The HEK293T cells plated in 6-well plate were transfected with two different concentrations of cloned miRNA cluster i.e 2micrograms and 4micrograms per well. Biological duplicates of 3 samples were used viz. control HEK293T cells, HEK293T cells transfected with 2micrograms of the cloned cluster and HEK293T cells transfected with 4micrograms of the cloned cluster.

2010-07-30 | E-GEOD-20158 | biostudies-arrayexpress

Integrating CRISPR knockout, interference, and activation to dissect the functional role and underlying signaling of microRNA-23a-27a-24-2 cluster in hepatocellular carcinoma

Project description:The miR-23a-27a-24-2 cluster is overexpressed in human cancers, including hepatocellular carcinoma (HCC). However, the role of three mature miRNAs of the miR-23a-27a-24-2 cluster in HCC is still controversial. Also, the integrative role of the miR-23a-27a-24-2 cluster in HCC remains elusive. In the present study, using CRISPR knockout (KO), CRISPR interference (CRISPRi), and CRISPR activation (CRISPRa) technologies, we established an endogenous miR-23a-27a-24-2 controllable and various knockout (KO) cell models, which were used to dissect the functional role and underlying signaling of the miR-23a-27a-24-2 cluster. Either miR-23a KO or miR-27a KO reduced cell growth in vitro and in vivo. Of particular note, endogenous miRNAs in the miR-23a-27a-24-2 cluster were effectively regulated by CRISPRi/a, identifying an integrated oncogenic role of the miR-23a-27a-24-2 cluster in HCC cells. Functional analysis showed that miR-23a KO and miR-27a KO led the cell cycle arrest, especially at the G2/M phase, by reducing CDK1/cyclin B activation in HCC cells. Furthermore, a high-throughput RNA-seq approach with miRNA target prediction identified the miR-23a/miR-27a-regulated gene network, further validated by various technologies. In addition, miR-23a and miR-27a have opposite roles in cell migration and mesenchymal-epithelial transition. However, an integrated analysis by CRISPRi/a suggested an oncogenic role of the miR-23a-27a-24-2 cluster in cell migration, which may require a miR-23a-BMPR2-Smad-Snail axis in HCC cells. Thus, our CRISPRi/a study offers a valuable research tool for dissecting the integrated role and underlying mechanism of an endogenous miRNA cluster. Also, this CRISPR approach may provide new routes of miRNA intervention for miRNA targeted therapy.

2024-09-30 | GSE199332 | GEO

The miR-23a~27a~24-2 microRNA cluster promotes inflammatory polarization of macrophages

Project description:The miR-23a~27a~24-2 microRNA cluster promotes inflammatory polarization of macrophages

| PRJNA670438 | ENA

Gene Expression in 70Z/3 pre-B cells Stably Overexpressing Individual members of the mirn23a MiRNA Cluster

Project description:Expression of the mirn23a cluster in murine hematopoietic progenitors blocks B cell development. Overexpressed individual cluster members miRs-23a, 24-2, and -27a in 70/3 mouse pre-B cells in order to examine changes in gene expression that would potentially reveal targets of the miRs relevant to hematopoiesis. Two independent 70Z/3 cell lines for each experimental group were generated (MSCV, miR-23a, miR-24-2, and miR-27a). RNA was generated and hybridized on Affymetrix microarrays.

2015-02-12 | E-GEOD-65874 | biostudies-arrayexpress

The miR-23a∼27a∼24-2 microRNA Cluster Promotes Inflammatory Polarization of Macrophages.

Project description:Macrophages are critical for regulating inflammatory responses. Environmental signals polarize macrophages to either a proinflammatory (M1) state or an anti-inflammatory (M2) state. We observed that the microRNA (miRNA) cluster mirn23a, coding for miRs-23a, -27a, and -24-2, regulates mouse macrophage polarization. Gene expression analysis of mirn23a-deficient myeloid progenitors revealed a decrease in TLR and IFN signaling. Mirn23a -/- bone marrow-derived macrophages (BMDMs) have an attenuated response to LPS, demonstrating an anti-inflammatory phenotype in mature cells. In vitro, mirn23a-/- BMDMs have decreased M1 responses and an enhanced M2 responses. Overexpression of mirn23a has the opposite effect, enhancing M1 and inhibiting M2 gene expression. Interestingly, expression of mirn23a miRNAs goes down with inflammatory stimulation and up with anti-inflammatory stimulation, suggesting that its regulation prevents locking macrophages into polarized states. M2 polarization of tumor-associated macrophages (TAMs) correlates with poor outcome for many tumors, so to determine if there was a functional consequence of mirn23a loss modulating immune cell polarization, we assayed syngeneic tumor growth in wild-type and mirn23a -/- mice. Consistent with the increased anti-inflammatory/immunosuppressive phenotype in vitro, mirn23a -/- mice inoculated with syngeneic tumor cells had worse outcomes compared with wild-type mice. Coinjecting tumor cells with mirn23a -/- BMDMs into wild-type mice phenocopied tumor growth in mirn23a -/- mice, supporting a critical role for mirn23a miRNAs in macrophage-mediated tumor immunity. Our data demonstrate that mirn23a regulates M1/M2 polarization and suggests that manipulation of mirn23a miRNA can be used to direct macrophage polarization to drive a desired immune response.

| S-EPMC7855803 | biostudies-literature

Gene Expression in 70Z/3 pre-B cells Stably Overexpressing Individual members of the mirn23a MiRNA Cluster

2015-02-12 | GSE65874 | GEO

Integrating CRISPR knockout, interference, and activation to dissect the functional role and underlying signaling of microRNA-23a-27a-24-2 cluster in hepatocellular carcinoma

Project description:Integrating CRISPR knockout, interference, and activation to dissect the functional role and underlying signaling of microRNA-23a-27a-24-2 cluster in hepatocellular carcinoma

| PRJNA819411 | ENA

CRISPR-based dissection of microRNA-23a ~ 27a ~ 24-2 cluster functionality in hepatocellular carcinoma.

Project description:The miR-23a ~ 27a ~ 24-2 cluster, commonly upregulated in diverse cancers, including hepatocellular carcinoma (HCC), raises questions about the specific functions of its three mature miRNAs and their integrated function. Utilizing CRISPR knockout (KO), CRISPR interference (CRISPRi), and CRISPR activation (CRISPRa) technologies, we established controlled endogenous miR-23a ~ 27 ~ a24-2 cell models to unravel their roles and signaling pathways in HCC. Both miR-23a KO and miR-27a KO displayed reduced cell growth in vitro and in vivo, revealing an integrated oncogenic function. Functional analysis indicated cell cycle arrest, particularly at the G2/M phase, through the downregulation of CDK1/cyclin B activation. High-throughput RNA-seq, combined with miRNA target prediction, unveiled the miR-23a/miR-27a-regulated gene network, validated through diverse technologies. While miR-23a and miR-27a exhibited opposing roles in cell migration and mesenchymal-epithelial transition, an integrated CRISPRi/a analysis suggested an oncogenic role of the miR-23a ~ 27a ~ 24-2 cluster in cell migration. This involvement potentially encompasses two signaling axes: miR-23a-BMPR2 and miR-27a-TMEM170B in HCC cells. In conclusion, our CRISPRi/a study provides a valuable tool for comprehending the integrated roles and underlying mechanisms of endogenous miRNA clusters, paving the way for promising directions in miRNA-targeted therapy interventions.

| S-EPMC11364504 | biostudies-literature

The miR-23a~27a~24-2 microRNA cluster promotes inflammatory polarization of macrophages

Project description:Purpose: RNA-sequencing was performed to identify gene expression changes between bone marrow derived macrophages isolated from wildtype and mirn23a-/- (Mirc11-/-) mice that were either M1 or M2 polarized. Results: Diferential gene expression was examined between wildtype and mirn23a-/- M1 polarized macrophages and wildtype and mirn23a-/- M2 polarized macrophages. The number of genes with significant (p<0.05) 2-fold changes in our M1 dataset is 4-fold higher than the 2-fold changed genes in our M2 dataset. 43 unique genes were differentially expressed over 2-fold in M1 mutant macrophages compared to wildtype with 29 upregulated and 14 downregulated. 10 genes (8 downregulated/ 2 upregulated)were differentially expressed in mirn23a-/- M2 macrophages by at least 2-fold compared to wildtype.

2020-11-18 | GSE159762 | GEO

The NF-?B p65/miR-23a-27a-24 cluster is a target for leukemia treatment.

Project description:p65 is a transcription factor that is involved in many physiological and pathologic processes. Here we report that p65 strongly binds to the miR-23a-27a-24 cluster promoter to up-regulate its expression. As bone marrow-derived cells differentiate into red blood cells in vitro, p65/miR-23a-27a-24 cluster expression increases sharply and then declines before the appearance of red blood cells, suggesting that this cluster is negatively related to erythroid terminal differentiation. Bioinformatic and molecular biology experiments confirmed that the miR-23a-27a-24 cluster inhibited the expression of the erythroid proteome and contributed to erythroleukemia progression. In addition, high level of the p65/miR-23a-27a-24 cluster was found in APL and AML cell lines and in nucleated peripheral blood cells from leukemia patients. Furthermore, anti-leukemia drugs significantly inhibited the expression of the p65/miR-23a-27a-24 cluster in leukemia cells. Administration of the p65 inhibitor parthenolide significantly improved hematology and myelogram indices while prolonging the life span of erythroleukemia mice. Meanwhile, stable overexpression of these three miRNAs in mouse erythroleukemia cells enhanced cell malignancy. Our findings thus connect a novel regulation pathway of the p65/miR-23a-27a-24 cluster with the erythroid proteome and provide an applicable approach for treating leukemia.

| S-EPMC4741785 | biostudies-literature

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