Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

VIRMA-mediated m6A modification profilling in human nasopharyngeal carcinoma

ABSTRACT: Several studies revealed an underlying disordered m6A regulatory network in human nasopharyngeal carcinoma (NPC). However, the roles of m6A regulators and sequential m6A dysregulation in NPC remain largely unknown. In the present study, we investigated the role of VIRMA and its underlying mechanisms in NPC. We performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) to identify the potential downstream targets of VIRMA that might be essential in NPC using HONE-1 cells with or without VIRMA silenced (two biological replicates).

ORGANISM(S): Homo sapiens

PROVIDER: GSE226363 | GEO | 2023/06/07

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

VIRMA-mediated m6A modification profilling in human nasopharyngeal carcinoma

Project description:VIRMA-mediated m6A modification profilling in human nasopharyngeal carcinoma

| PRJNA940069 | ENA

WTAP-mediated m6A modification profiling in human nasopharyngeal carcinoma cell lines

Project description:N(6)-methyladenosine (m6A) plays an important role in the tumorigenesis and progression of cancers. However, the clinical significance of m6A and their regulatory mechanisms in nasopharyngeal carcinogenesis (NPC) remain largely unknown. In this study, we used the microarray analysis to study WTAP-mediated m6A modification profiles in human nasopharyngeal carcinoma cell line, HONE-1, by comparing 3 pairs of samples with or without WTAP knockdown.

2022-06-15 | GSE160644 | GEO

The m6A-enriched lncRNA LINC00839 promotes tumor progression by binding TAF15 and activate AOC1 transcription in nasopharyngeal carcinoma [RNA-seq]

Project description:Dysregulations of long non-coding RNAs (lncRNA) contribute to tumorigenesis by modulating specific cancer-related pathways, but the roles of m6A-enriched lncRNAs and underlying mechanisms remain elusive in nasopharyngeal carcinoma (NPC). Here, we reanalyzed the previous genome-wide analysis of lncRNA profile, and discerned that an oncogenic m6A-enriched lncRNA, LINC00839, which was substantially upregulated in NPC and correlated with poor clinical prognosis, promoted NPC growth and metastasis in vitro and in vivo. Mechanistically, LINC00839 interacted directly with transcription factor, TATA-box binding protein associated factor (TAF15), and coordinated its recruitment to promoter region of amine oxidase copper-containing 1 (AOC1), thereby activating AOC1 transcription in trans. Ectopic expression of AOC1 partially rescued the inhibitory effect of downregulation of LINC00839 in NPC. Furthermore, silencing vir like m6A methyltransferase associated (VIRMA) and insulin-like growth factor 2 mRNA-binding proteins 1 (IGF2BP1) were found to attenuate the expression level and RNA stability of LINC00839 in an m6A-dependent manner. This study unveils a novel oncogenic VIRMA/IGF2BP1–LINC00839–TAF15–AOC1 axis, and highlights significance and prognostic value of LINC00839 in NPC carcinogenesis.

2023-07-05 | GSE228724 | GEO

The m6A-enriched lncRNA LINC00839 promotes tumor progression by binding TAF15 and activate AOC1 transcription in nasopharyngeal carcinoma [ChIP-Seq]

2023-07-05 | GSE228723 | GEO

Induced of RBM24 expression effect on nasopharyngeal carcinoma cells

Project description:RNA-binding proteins (RBPs) are key components in the determination of miRNA function, as they control different stages of miRNA biogenesis and their localization, degradation and activity. To further investigate the underlying mechanisms of RBM24 in nasopharyngeal carcinoma (NPC) carcinogenesis, we compared the miRNA expression profiles in RBM24 induced and control cells by using human miRNA microarray. Microarray analysis identified 11 commonly upregulated and 12 commonly downregulated miRNAs in RBM24 induced cells. Among the 23 miRNAs, miR-25 ranked highest of all the commonly upregulated genes sorted in ascending order according to fold change values. RBM24 expression was controlled by tetracycline-off system in NPC cells. microRNA profiling of RBM24 expression induced cells vs. repressed cells: The expression of RBM24 in HONE-1, 5-8F, and CNE-2 cells was induced by removing doxycycline or repressed by adding doxycycline.

2016-03-13 | E-GEOD-66878 | biostudies-arrayexpress

VIRMA-mediated m6A modification regulates forebrain formation through facilitating ribosome biogenesis

Project description:N6-methyladenosine (m6A) modification plays crucial roles in tissue development and homeostasis. However, the mechanisms underlying cellular adaptation of m6A modification and their impact on protein synthesis machinery remain unclear. VIRMA, the largest and evolutionarily conserved core of the m6A methyltransferase complex, is highly expressed in the embryonic brain and various cancers. Here, we demonstrate that VIRMA-mediated m6A modification is essential for active ribosome biogenesis. VIRMA depletion destabilizes the entire writer complex and reduces m6A levels, leading to decreased proliferation and increased apoptosis of neural progenitor/stem cells (NPCs), ultimately causing severe forebrain developmental defects. Mechanistically, VIRMA depletion impairs ribosome biogenesis by inhibiting mRNA decay, triggering a p53-dependent stress response and compromising global protein synthesis. Importantly, these findings extend to human cancer cells, suggesting a potential conservation of this mechanism. Overall, our study reveals the critical role of m6A in adapting protein synthesis machinery during brain development and potentially in cancer.

2024-10-29 | GSE279759 | GEO

VIRMA-mediated m6A modification regulates forebrain formation through facilitating ribosome biogenesis

2024-10-31 | GSE279609 | GEO

Effect of Overexpression of VIRMA on m6A-methylated mRNAs in breast cancer cells

Project description:To identify m6A-regulated mRNA targets affected by VIRMA overexpression we compared m6A peak abundance measured via m6A RNA immunoprecipitation sequenc-ing in SKBR3 cells overexpressing full-length VIRMA and eGFP control

2023-08-03 | GSE205892 | GEO

Long non-coding RNAs and mRNAs expression profilling in human nasopharyngeal carcinoma

Project description:Long non-coding RNAs (lncRNAs) play important roles in the tumorigenesis and progression of cancers. However, the clinical significance of lncRNAs and their regulatory mechanisms in nasopharyngeal carcinogenesis (NPC) are largely unknown. In this study, we used the microarray analysis to study the different expression profiles of lncRNAs and mRNAs in human nasopharyngeal carcinoma tissues. We performed genome-wide lncRNAs expression in 3 pairs of NPC and normal nasopharynx tissues and identified 384 dysregulated lncRNAs (fold change ≥2 and P <0.05).

2019-09-30 | GSE126683 | GEO

KIAA1429/VIRMA promotes breast cancer proliferation and migration by stabilizing m6A-modified HAS2 RNA expression in cytosol

Project description:N6-methyladenosine (m6A) is the most abundant internal RNA modification in mRNA molecules and plays important roles in multiple important biological processes including cancer development. KIAA1429/VIRMA is an important component of m6A methyltransferase complex to facilitate depositing m6A modification in RNA molecules. Here we found that KIAA1429/VIRMA was overexpressed in breast cancer patients among other m6A related enzymes. Breast cancer patients with higher KIAA1429 expression have worse survival compared with control group. In addition, KIAA1429/VIRMA protein mislocated in cytosol in breast cancer tissues and cell lines. KIAA1429/VIRMA depletion reduced breast cancer cell proliferation and migration. Mechanism studies showed that cytosolic expressed KIAA1429/VIRMA interacted with m6A reader protein IGF2BP3 and stabilized expression of m6A-modified HAS2 expression. HAS2 is downstream of KIAA1429/VIRMA to mediate breast cancer cell proliferation and migration and has positive correlation with KIAA1429/VIRMA expression in cancer patients.

2021-11-02 | GSE185494 | 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