Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles of WDR4 knockdown in HCC cells

ABSTRACT: HCC cell line, Huh-7 cells and HCC-LM3 cells, was transfected with sh-WDR4-2 or sh-NC for 48hr to knockdown WDR4 expression, and check the downstream mRNA changes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE169394 | GEO | 2021/07/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiles of METTL5-Wild type(WT) knockout(KO) in HCC cells

Project description:HCC cell line, Huh-7 cells and HCC-LM3 cells, was transfected with METTL5 sgRNA to knockout METTL5 expression., and check the downstream mRNA changes.

2023-01-06 | GSE203329 | GEO

Gene expression profiles of PML knockdown or WDR4 overexpression in A549 cells

Project description:Lung cancer cell line, A549 cells, was transfected with siPML or siCtrl for 48hr to knockdown PML expression. WDR4 or vector was overexpressed in A549 cells for 48hr. These four sets of cells were then subjected to microarray profiling using the Human OneArray microarray (version HOA6.1, GEO Platform GPL19137) from Phalanx Biotech Group. Comparison of transcriptomes from siPML/siCtrl and W4/vec in A549 cells

2016-07-04 | E-GEOD-83499 | biostudies-arrayexpress

Gene expression profiles of PML knockdown or WDR4 overexpression in A549 cells

2016-07-04 | GSE83499 | GEO

Gene expression profiles of WDR4 knockdown in HCC cells

Project description:Gene expression profiles of WDR4 knockdown in HCC cells

| PRJNA716516 | ENA

MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) Human HCC proteomics

Project description:The long noncoding RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), also known as MALAT-1 or NEAT2 (nuclear-enriched abundant transcript 2), is a highly conserved nuclear noncoding RNA (ncRNA). Two molecular functions of MALAT1 have been proposed, one is the control of alternative splicing and the other is the transcriptional regulation. To uncover its function in HCC, we knock down it in human HCC LM3 cell lines, and profiling the sample with LC/MS/MS and RNA sequencing.

2021-09-21 | PXD016790 | Pride

The effect of K458R mutation of HNF4A on HCC

Project description:To investigate the inhibitory effect of K458R mutation of HNF4A on HCC, we established Huh-7 xenografts treated with Ad-GFP, Ad-HNF4A or Ad-K458R. We then performed gene expression profiling analysis using data obtained from RNA-seq of three groups of Huh-7 xenografts treated with adenovirus.

2023-02-20 | GSE225329 | GEO

Effect of FENDRR on genetic expressions of primary liver cancer based on next generation sequencing

Project description:Primary liver cancer (PLC) is the third largest contributor to cancer mortality in the world. PLC is a heterogeneous disease that encompasses several biologically distinct subtypes including hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and combined hepatocellular-cholangiocarcinoma (CHC). The cells were cultured in DMEM medium supplemented with 10% fetal bovine serum and 1% antibiotic-antimitotic solution. The HCC cell line LM3 and ICCA cell line RBE were transfected using Lipofectamine 3000 reagent following the manufacturer’s protocol and incubated for 48h for further analysis. The gene expression profiles were analyzed of LM3 and RBE cells transfected with si-FENDRR or si-NC to assess effect of FENDRR on genetic expressions of PLC.

2021-03-15 | GSE168885 | GEO

WDR4 conditional knockout in mouse cerebellar granule progenitors for proteome analysis

Project description:To uncover candidates which are WDR4 downstream effectors regulating cerebellar granule neuron proliferation phenotype, we utilized quantitative proteomics analysis (TMT labeling) with granule neuron progenitors from P7 wdr4 conditional knockout (using Atoh1-Cre) and control cerebella.

2023-03-11 | PXD022319 | Pride

m7G Trac-Seq analysis in MEF Wt cells overexpressing METTL1+WDR4

Project description:The RNA methyltransferase METTL1 catalyzes the N7-methylguanosine (m7G) modification of certain tRNAs, mRNAs, and miRNA precursors. However, the role of METTL1 and its cofactor WDR4 in cancer remains largely unexplored. Here we reveal the oncogenic role of METTL1/WDR4. METTL1 is frequently amplified and overexpressed in cancers and correlates with poor patient survival. METTL1 depletion in human cancer cells causes decreased abundance of m7G-modified tRNAs, altered cell cycle, and inhibits oncogenicity. Strikingly, METTL1/WDR4 overexpression induces oncogenic transformation and carcinogenesis. Mechanistically, we find increased abundance of a subset of m7G-modified tRNAs including tRNA-Arg(TCT), and increased translation of mRNAs enriched in the corresponding AGA codon including cell cycle regulators. Accordingly, expression of tRNA-Arg(TCT) is significantly elevated in many cancer types, correlates with patient survival, and overexpression of this tRNA enhances reporter gene expression and cell transformation. Thus, METTL1/WDR4-mediated m7G tRNA modification drives oncogenic transformation, thereby highlighting METTL1 as a promising cancer therapeutic target.

2020-10-01 | GSE149950 | GEO

PTPN23 ubiquitination by WDR4 suppresses EGFR and c-MET degradation to define a lung cancer therapeutic target

Project description:Aberrant overexpression or activation of EGFR drives the development of non-small cell lung cancer (NSCLC) and acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) by secondary EGFR mutations or c-MET amplification/activation remains as a major hurdle for NSCLC treatment. We previously identified WDR4 as a substrate adaptor of Cullin 4 ubiquitin ligase and an association of WDR4 high expression with poor prognosis of lung cancer. Here, using an unbiased ubiquitylome analysis, we uncover PTPN23, a component of the ESCRT complex, as a substrate of WDR4- based ubiquitin ligase. WDR4-mediated PTPN23 ubiquitination leads to its proteasomal degradation, thereby suppressing lysosome trafficking and degradation of wild type EGFR, EGFR mutant, and c-MET. Through this mechanism, WDR4 sustains EGFR and c-MET signaling to promote NSCLC proliferation, migration, invasion, stemness, and metastasis. Clinically, PTPN23 is downregulated in lung cancer and its low expression correlates with WDR4 high expression and poor prognosis. Targeting WDR4-mediated PTPN23 ubiquitination by a peptide that competes with PTPN23 for binding WDR4 promotes EGFR and c-MET degradation to block the growth and progression of EGFR TKI-resistant NSCLC. These findings identify a central role of WDR4/PTPN23 axis in EGFR and c-MET trafficking and a potential therapeutic target for treating EGFR TKI-resistant NSCLC.

2023-10-09 | PXD025361 | Pride

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