Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of miR-34a overexpression on the transcriptome of HEK293T cells

ABSTRACT: MicroRNAs regulate gene expression post-transcriptionally through binding to target sites in mRNAs. Predictions of target site efficiency are limited by our understanding of the structure-function relationship of microRNA-target complexes. Here, we overexpressed miR-34a in HEK293T cells and performed RNA-sequencing in order to study how different structural features of predicted miRNA-target complexes correlate with changes in gene expression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE274168 | GEO | 2025/07/23

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of miR-34a overexpression on the transcriptome of HEK293T cells

Project description:Effect of miR-34a overexpression on the transcriptome of HEK293T cells

| PRJNA1145337 | ENA

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

NCI-H1299 lung cancer cell line transfected with miR-34a and ghR-34a

Project description:Analysis NCI-H1299 lung cancer cells transfected with synthetic oligo mimics for microRNAs (miRNAs) miR-34a and ghR-34a. We developed a 30-nucleotide single-strand RNA (ssRNA), termed “guide hairpin RNA (ghR),” that has a physiological function similar to that of miRNA and siRNA. The ghR caused no innate cytokine response either in vitro or in vivo. In addition, its structure does not contain a passenger strand seed sequence, reducing the potential for off-target effects relative to existing short RNA reagents. Systemic injection of ghR-form miR-34a (ghR-34a) suppressed tumor growth in a mouse model of RAS-induced lung cancer. Furthermore, ghR-34a functioned in a Dicer- and Ago2-independent manner. This novel RNAi technology may provide a novel, safe, and effective nucleic acid drug platform that will increase the clinical usefulness of nucleic acid therapy. MiR-34a–targeted mRNAs regulated by mRNA degradation rather than translational inhibition were identified using microarray data from miR-34 and ghR-34a transfectants.

2015-07-29 | E-GEOD-71423 | biostudies-arrayexpress

NCI-H1299 lung cancer cell line transfected with miR-34a and ghR-34a

2015-07-29 | GSE71423 | GEO

Comparing two approaches of miR-34a target identification, biotinylated-miRNA pulldown vs miRNA overexpression

Project description:Here we show that biotin-labelled miR-34a can be loaded to AGO2, and AGO2 immunoprecipitation can pulldown biotinylated miR-34a (Bio-miR pulldown). RNA-sequencing (RNA-seq) of the Bio-miR pulldown RNAs efficiently identified miR-34a mRNA targets, which could be verified with luciferase assays. In contrast to the approach of Bio-miR pulldown, RNA-seq of miR-34a overexpression samples had limited value in identifying direct targets of miR-34a. It seems that pulldown of 30 -Biotin-tagged miRNA can identify bona fide microRNA targets at least for miR34a.

2019-02-27 | GSE127211 | GEO

Overexpression of USF1 in HEK293T cells

Project description:Overexpression of USF1 in HEK293T cells in vitro to ascertain the genes downstream of USF1. Will identify direct targets as well as indirect targets of USF1. Keywords: Overexpression of transcription factor to determine downstream targets. Cloned USF1 from cDNA and transiently transfected into HEK293T cells. Total RNA collected 48 hours after transfection. Empty vector used as control. Expression of USF1 was validated using western blot, and qRT-PCR was used to validate differential expression.

2009-09-14 | E-GEOD-17300 | biostudies-arrayexpress

A global transcriptome analysis of human epidermal keratinocytes upon overexpression of microRNA-34a or microRNA-34c

Project description:miR-34a and miR-34c were found up-regulated at wound-edges of human venous ulcer compared to nomal wound and the intact skin; however their biological role in keratinocytes during wound repair has not been studied. To study the genes regulated by miR-34a and miR-34c, we transfected miR-34a and miR-34c mimic into human primary epidermal keratinocytes to overexpress them. We performed a global transcriptome analysis of keratinocytes upon overexpression of miR-34a or miR-34c using Affymetrix arrays.

2019-09-04 | GSE117506 | GEO

Comparison of normal and KCNQ3 overexpressing HEK293T cells

Project description:KCNQ3 (KQT-like potassium channel member 3) was overexpressed in HEK293T cells and compared to control

2022-06-01 | GSE152673 | GEO

CLASH for 15.5K and FBL proteins in HEK293T cells

Project description:We performed CLASH for 15.5K and FBL in HEK293T cells which overexpressed 15.5K and FBL, respectively.

2023-04-10 | GSE160636 | GEO

ChIP-seq on ZNF506 overexpression HEK293T to verify ZNF506 binding capacity at PBS-Pro sites.

Project description:To identify ZNF506 genome-wide target sites, we performed ChIP-seq assay and found that ZNF506 binding sites enriched at PBS-Pro-containing ERV subfamilies (ERVPs) and further motif calling analysis showed that ZNF506 binds to PBS-Pro sequences, promoting formation of H3K9me3 modifications at binding regions. And ChIP-seq assay also indicated that the distinction of H3K9me3 signals closed to ZNF506 peak regions between ZNF506 overexpressing (OE) HEK293T cells and ZNF506 Knockout (KO) HEK293T cells was correlated with the different recruitment of corepressor KAP1. The ChIP-seq experiments using GFP antibodies and H3K9me3 antibodies on ZNF506-GFP OE HEK293T cell lines, and ZNF417-GFP OE HEK293T cell lines were used as controls for H3K9me3 ChIP. Also, the ChIP-seq experiments were performed using H3K9me3 antibodies and KAP1 antibodies on ZNF506 KO HEK293T cells and ZNF506 OE HEK293T cells.

2023-07-26 | GSE209826 | 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