Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of knockdown of KIAA1429 on gene expression in HepG2 cells

ABSTRACT: Effect of knockdown of KIAA1429 on gene expression in HepG2 cells

PROVIDER: PRJNA985622 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR24968126.fastq.gz	Fastqsanger.gz
	SRR24968127.fastq.gz	Fastqsanger.gz
	SRR24968128.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Effect of knockdown of KIAA1429 on gene expression in HepG2 cells

Project description:Total RNA was extracted from HepG2 cells with si-NC (N=2) or si-KIAA1429 (N=2). To investigate the global genes which were regulated by KIAA1429, high-throughput mRNA sequencing (RNA-Seq) was performed to compare the expression profile in HepG2 cells.

2025-06-19 | GSE235253 | GEO

Effect of ZFP740 knockdown on HepG2 cells

Project description:Effect of ZFP740 knockdown on HepG2 cells

| PRJNA1117433 | ENA

HepG2 TP53BP2-knockdown

Project description:HepG2 TP53BP2-knockdown

| PRJNA854656 | ENA

The effect of KIF11 knockdown on gene expression profile in HepG2 cells

Project description:The effect of KIF11 knockdown on gene expression profile in HepG2 cells

| PRJNA998071 | ENA

HepG2 HepAD38 TP53BP2-knockdown

Project description:HepG2 HepAD38 TP53BP2-knockdown

| PRJNA854649 | ENA

Gene expression profiling of ATP9A knockdown HepG2 cells

Project description:Gene expression profiling of ATP9A knockdown HepG2 cells

| PRJNA508627 | ENA

Effect of ZFP740 knockdown on HepG2 cells

Project description:To investigate the effect of ZFP740 gene expression on hepatocellular carcinoma cells, we used the hepatocellular carcinoma cell line HepG2, and then divided into two groups, in which the control group was HepG2, and the intervention group was HepG2 with the knockdown of the ZNF740 gene, and three samples were sent to each group for RNA seq sequencing

2024-07-04 | GSE268479 | GEO

KIAA1429 promotes cell proliferation by regulating MYC messenger RNA in clear cell renal cell carcinoma

Project description:KIAA1429 is an integral component of the m6A methyltransferase complex, essential for facilitating the interaction between the catalytic core components METTL3 and METTL14. However, the mechanisms by which KIAA1429 influences clear cell Renal cell carcinoma (ccRCC) remain incompletely elucidated. Analysis of the TCGA and GEO database confirmed that KIAA1429 was significantly upregulated in ccRCC samples, which correlated with poor survival. Additionally, qRT-PCR, Western Blot and IHC detection revealed significantly upregulated levels of KIAA1429 in ccRCC tissues. Moreover, multivariable Cox regression analysis showed that patients with ccRCC with high KIAA1429 expression had a poor clinical prognosis. Notably, silencing KIAA1429 significantly inhibited the proliferation, migration and invasion of ccRCC cells. Similarly, KIAA1429 knockdown also significantly inhibited the growth of ccRCC cells in nude mice. Mechanistically, KIAA1429 silencing significantly reduced the overall level of m6A in, the stability of MYC mRNA and the mRNA and protein expressions of MYC in ccRCC cells. Furthermore, RIP-qRT-PCR experiments showed that KIAA1429 could directly bind to MYC mRNA. MeRIP assay revealed that KIAA1429 knockdown resulted in a significant decrease in the m6A level of MYC mRNA in ccRCC cells. In conclusion, KIAA1429 regulates the proliferation, migration and invasion of ccRCC cells by stabilizing MYC mRNA in an m6A-dependent manner. Therefore, targeting the KIAA1429-MYC signalling pathway emerges as a potential strategy for the treatment of renal cell carcinoma.

2024-09-10 | GSE276431 | GEO

Effect of SPARC on gene expression in HepG2

Project description:Effect of SPARC on gene expression in HepG2

| PRJNA704276 | ENA

Genome-wide identification of transcripts associated with KIAA1429 by RIP-seq

Project description:N6-methyladenosine (m6A) modification, as the most abundant internal methylation of eukaryotic RNA transcripts, is critically implicated in RNA processing, decay, transport and translation. Here we showed that KIAA1429, the largest known component in the m6A methyltransferase complex, was considerably upregulated in hepatocellular carcinoma (HCC) tissues. High expression of KIAA1429 was significantly associated with the malignant clinical features and the poor prognosis of HCC patients. Silencing KIAA1429 suppressed the cell proliferation and metastasis in vitro and in vivo. Integrated MeRIP-seq, RIP-seq and RNA-seq data identified GATA3 as the direct downstream target of KIAA1429-mediated m6A modification. KIAA1429 knockdown markedly impaired the m6A levels of GATA3 mRNA and increased the expression of GATA3. Mechanistically, KIAA1429 induced the m6A methylation on 3’ UTR of GATA3 pre-mRNA, leading to the separation of RNA-binding protein HuR and the degradation of GATA3 pre-mRNA, which was followed by the downregulation of GATA3. Strikingly, a long noncoding RNA (lncRNA) GATA3-AS, transcribed from the antisense strand of GATA3 gene, functioned as a cis-acting element for the preferential interaction of KIAA1429 with GATA3 pre-mRNA. Accordingly, we found that the tumor growth and metastasis driven by KIAA1429 or GATA3-AS were mediated by GATA3. Patients with low KIAA1429 and high GATA3 expressions showed greatly better poor overall survival and disease-free survival. In conclusion, our study proposed a complex KIAA1429-GATA3 regulatory model based on m6A modification and provided insights into the epi-transcriptomic dysregulation in hepatocarcinogenesis and metastasis.

2019-07-27 | GSE134978 | 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