Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA stability profiling in SETD2 and METTL14 knockdown HepG2 cells

ABSTRACT: To evaluate the effect of SETD2 and METTL14 on mRNA stability, we conducted RNA-seq in SETD2 or METTL14 knockdown HepG2 cells as well as control cells with or without actinomycin D treatment. Our RNA stability profiling revealed that depletion of SETD2 and METTL14 resulted in global reduction of RNA stability, and the changes were correlated between SETD2 and METTL14 knockdown cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE121949 | GEO | 2019/02/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

RNA stability profiling in SETD2 and METTL14 knockdown HepG2 cells

Project description:RNA stability profiling in SETD2 and METTL14 knockdown HepG2 cells

| PRJNA499122 | ENA

Active ribosome profiling in SETD2 or METTL14 knockdown HepG2 cells

Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL14 is a critical subunit of the m6A methyltransferase complex. To evaluate the effect of SETD2 and METTL14 on translation, we conducted robosome profiling in SETD2 and METTL14 knockdown and control HepG2 cells. Our RNA ribosome profiling revealed that depletion of SETD2 and METTL14 resulted in a global reduction in RNA translation and the changes of translation efficiency were correlated between SETD2 and METTL14 knockdown cells.

2019-02-21 | GSE121952 | GEO

Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL3, METTL14 and WTAP are the components of m6A methyltransferase complex. To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 and METTL3, METTL14 or WTAP knockdown HepG2 cells, and found depletion of H3K36me3 by SETD2 silencing globally reduced m6A in human transcriptome. What’s more, most of the SETD2-dependent hypomethylation sites also responded to knockdown of METTL3, METTL14, or WTAP.

2019-02-21 | GSE110320 | GEO

Active ribosome profiling in SETD2 or METTL14 knockdown HepG2 cells

Project description:Active ribosome profiling in SETD2 or METTL14 knockdown HepG2 cells

| PRJNA501872 | ENA

IGF2BP proteins Enhance mRNA stability

Project description:To evaluate the effect of IGF2BPs on mRNA stability and gene expression output, we conducted RNA-seq in individual IGF2BP knockdown and control HepG2 cells with or without actinomycin D treatment. Our RNA-seq and RNA stability profiling revealed that IGF2BPs were involved in RNA stability regulation and contributed to the stabilization of the transcriptome.

2018-03-15 | GSE90684 | GEO

Setd2 knockdown.

Project description:Setd2 knockdown.

| PRJNA612891 | ENA

Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

Project description:Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

| PRJNA433472 | ENA

Knockdown of METTL14 inhibits the development of neuroblastoma

Project description:We investigated the mechanism by which the m6A methyltransferase METTL14 functions in neuroblastoma. To explore the downstream target genes of METTL14, we performed RNA-seq analysis and found that the expression profile of the gene was significantly altered in METTL14 knockdown SK-N-BE(2) cells. We found that overexpression of METTL14 in neuroblastoma patients was a detrimental factor.

2024-04-02 | GSE244657 | GEO

N6-methyladenosine methyltransferase METTL14-mediated autophagy in malignant development of oral squamous cell carcinoma

Project description:N6-methyladenosine (m6A) is the most abundant internal mRNA modification in eukaryotes and is related to stability, localization, or translation efficiency in tumorigenesis. Autophagy plays an important role in the occurrence and development of tumours. However, the relationship between m6A and autophagy remains unclear. In this study, we used a rapamycin-induced autophagy model of oral squamous cell carcinoma (OSCC) cells, and observed increased m6A RNA methylation. When autophagy was activated, the methyltransferase-like 14 (METTL14) expression was upregulated and influenced the proliferation, migration, and invasiveness of OSCC cells. Through meRIP-seq and RNA-seq analysis, we found that METTL14 directly combined with eukaryotic translation initiation factor gamma 1 (eIF4G1) mRNA and decreased its RNA stability. According to the dual-luciferase reporter and mutagenesis assay, the mutated site 1 of exon 11 of eIF4G1 is the key target of METTL14. Knockdown of the main m6A binding protein YTHDF2 may rescue the shortened half-life of eIF4G1 mRNA induced by METTL14 overexpression. Furthermore, an in vivo tumour xenograft model confirmed that a high METTL14 expression can effectively reduce OSCC growth. Additionally, using clinical samples, we found that patients with advanced or moderately/poorly differentiated tumours exhibited lower METTL14 levels. Taken together, our results revealed that METTL14 mediated eIF4G1 expression via m6A modification and regulated autophagy levels and biological functions in OSCC. Our findings not only expand our understanding of the correlation between autophagy and RNA methylation in tumorigenesis but also present an opportunity to develop new therapeutic options.

2021-11-17 | GSE186581 | GEO

RNA Methyltransferase METTL14 Promotes Breast Cancer Growth and Progression

Project description:We investigated the role of RNA N6-adenosine methyltransferase protein METTL14 that supports breast cancer growth and progression, and we showed METTL14 knockdown inhibited long-term survival, migration as well as invasion of breast cancer cells.

2018-12-26 | GSE81164 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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