Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The METTL3 RNA methyltransferase regulates gene expression in castrate resistant LNCaP:C42 prostate cancer cells

ABSTRACT: The METTL3 RNA methyltransferase regulates gene expression in castrate resistant LNCaP:C42 prostate cancer cells

PROVIDER: PRJNA801594 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17803624_1.fastq.gz	Fastqsanger.gz
	SRR17803624_2.fastq.gz	Fastqsanger.gz
	SRR17803625_1.fastq.gz	Fastqsanger.gz
	SRR17803625_2.fastq.gz	Fastqsanger.gz
	SRR17803626_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

The METTL3 RNA methyltransferase regulates androgen signalling in castrate resistant prostate cancer cells

Project description:iRNAs targeting METTL3 used to deplete METTL3 in castrate resistant LNCaP:C42 and 22Rv1 prosate cancer cells and the effect on basal and androgen regulated gene expression and splicing determined.

2022-11-02 | GSE194420 | GEO

Clinical and molecular significance of the RNA m6A methyltransferase complex in prostate cancer

Project description:shRNAs targeting METTL3 used to deplete METTL3 in castrate-resistant LNCaP:C42 prostate cancer cells and the effect on gene expression and splicing determined.

2023-01-04 | GSE210130 | GEO

The METTL3 RNA methyltransferase regulates androgen signalling in castrate resistant prostate cancer cells

Project description:The METTL3 RNA methyltransferase regulates androgen signalling in castrate resistant prostate cancer cells

| PRJNA800457 | ENA

The METTL3 RNA methyltransferase regulates gene expression in castrate resistant 22Rv1 prostate cancer cells

Project description:The METTL3 RNA methyltransferase regulates gene expression in castrate resistant 22Rv1 prostate cancer cells

| PRJNA801508 | ENA

The METTL3 RNA methyltransferase regulates gene expression in castrate resistant LNCaP:C42 prostate cancer cells

Project description:RNA sequencing was used to determine the effect of the STM2457 METTL3 inhibitor on prostate cancer cell gene expression.

2022-11-02 | GSE195632 | GEO

Proteomic analysis of castrate resistant prostate cancer cell lines

Project description:In this study the development of androgen independence in a cell model of disease was selected as a mirror of to the events at play in the development of Castrate Resistant Prostate Cancer in-vivo. LNCaP cells which are androgen dependent and androgen independent sublines; LNCaP-Abl and LNCaP-Abl-Hof were subject to extensive fractionation by 1-D SDS PAGE and accurate mass-high resolution mass spectrometry (Q Exactive) to identify proteins whose expression was changes significantly in response to androgen independent growth.

2022-02-28 | PXD000751 | Pride

The METTL3 RNA methyltransferase regulates gene expression in castrate resistant 22Rv1 prostate cancer cells

Project description:RNA sequencing was used to determine the effect of the STM2457 METTL3 inhibitor on prostate cancer cell gene expression.

2022-11-02 | GSE195624 | GEO

Gene expression signature of castrate resistant prostate cancer

Project description:Prostate gland is a highly androgen dependent gland. The first line of treatment for metastatic prostate cancer therefore, is androgen ablation. This can be achieved by multiple non-surgical methods. However, most of these cancers although respond well initially, become resistant to androgen ablation sooner or later. These cancers then become extremely aggressive and difficult to treat, thereby drastically affect the patient prognosis. A gene expression signature for castrate resistant prostate cancer would be useful in identification of mechanisms responsible for castrate resistance, as well as to predict the progression of the cancer into castrate resistance. For this, our group has done a RNA-seq analysis of a. Control group (C); b. Castrate Sensitive group (B) and c. Castrate Resistant group (A). Gene expression profiling was performed on these samples using RNA-seq. Differentially expressed genes between control and castrate sensitive as well as control and castrate resistant groups were identified.

2024-09-11 | GSE262940 | GEO

m6A methyltransferase METTL3 regulates Tfh cell differentiation

Project description:m6A methyltransferase METTL3 regulates Tfh cell differentiation

| PRJNA532389 | ENA

Chromatin-occupancy profiling of PRMT5 and METTL3 in prostate cancer cells

Project description:Prostate cancer (PCa) is the most frequently diagnosed malignancy in men worldwide. Epigenetic regulation has been recognized as a main mechanism of cancer evolution. PRMT5 is the major type II protein arginine methyltransferase catalyzing the symmetric dimethylation of arginine, and METTL3 is the enzymatic component of the large N6-adenosine-methyltransferase complex in mammalian responsible for N6-methyladenosine (m6A) modification in diverse RNA species. Both genes are found upregulated in PCa. However, their exact functional contribution to prostate tumorigenesis is unknown. As both proteins can regulate transcription via binding to chromatin, we seek to explore their DNA binding profiles in both AR+ LNCaP and AR- PC3 cells via recently developed CUT&Tag technique. Antibodies we used were Active Motif #61001 for PRMT5 and Abcam #195352 for METTL3. Our data suggests that both proteins regulate PCa cell biology, at least partially, through chromatin-binding and subsequent transcriptional regulation. CUT&Tag assay for arginine methyltransferase PRMT5 and N6‐adenosine‐methyltransferase METTL3 in LNCaP and PC3 cells

2024-09-03 | GSE217412 | 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