Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: Effect of SF3B1 suppression in cancer cells with different SF3B1 copy-number levels

PROVIDER: PRJNA323711 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR3605490_1.fastq.gz	Fastqsanger.gz
	SRR3605490_2.fastq.gz	Fastqsanger.gz
	SRR3605491_1.fastq.gz	Fastqsanger.gz
	SRR3605491_2.fastq.gz	Fastqsanger.gz
	SRR3605492_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Effect of SF3B1 suppression in cancer cells with different SF3B1 copy-number levels

Project description:Breast cancer cell lines containing stable dox inducible shRNAs targeting SF3B1 were profiled by RNA sequencing. We determined the effect of gene expression and splicing changes before and after knocking down SF3B1 in cell lines with normal copy number (SF3B1neutral) or partial copy loss (SF3B1loss) cell lines

2017-02-07 | GSE81978 | GEO

Homo sapiens

Project description:The histotype-specific copy-number landscape of ovarian cancer (copy number SNP)

| PRJNA155145 | ENA

Homo sapiens

Project description:The histotype-specific copy-number landscape of ovarian cancer (copy number Japan)

| PRJNA154789 | ENA

Homo sapiens

Project description:Male breast cancer copy number profiles

| PRJNA245407 | ENA

Homo sapiens

Project description:Copy number profiling of ovarian cancer ascitic effusion

| PRJNA140169 | ENA

Homo sapiens

Project description:Copy number profiling of PE ovarian cancer lines

| PRJNA118183 | ENA

Homo sapiens

Project description:Multisampled Lethal Metastatic Prostate Cancer Copy Number Analysis

| PRJNA111809 | ENA

Homo sapiens

Project description:Germline copy number variations and breast cancer risk

| PRJNA674608 | ENA

RNAseq data to study PRPF6 regulated splice forms in colon cancer cell lines

Project description:Description Alternative splicing plays critical roles in differentiation, development, and cancer. Using an integrated genomic approach, we have identified PRPF6, an RNA binding component of the pre-mRNA spliceosome, as an essential driver of oncogenesis in colon cancer. Importantly, PRPF6 is both amplified and overexpressed in colon cancer, and only colon cancer cells with high PRPF6 levels are sensitive to its loss. Our data clearly point to an important role for PRPF6 in colon cancer growth and suggest that a better understanding of its role in alternative splicing in colon cancer is warranted. To determine the specific alternative splice forms that PRPF6 regulates in colon cancer, we conducted the following experiment: Using two colon cancer cell lines (KM-12 and SW620) that have high PRPF6 levels, we inhibited PRPF6 expression using 2 independent siRNAs. We also tested the effect of U2 snRNP inhibition using both a siRNA targeting SF3B1 as well as spliceostatin A (a small molecule inhibitor of SF3B1). We then conducted RNA-seq to determine the gene expression and exonic changes that occur relative to either the non-targeting control siRNA (for siSF3B1 and siPRPF6) or the vehicle control (for spliceostatin A).

2014-05-10 | E-MTAB-2505 | biostudies-arrayexpress

Long-read sequencing of CLL and MDS patients uncovers molecular effects of SF3B1 mutations in cancer (SF3B1 & U2AF2 iCLIP)

Project description:Alternative splicing plays a critical role in generating transcriptome diversity, and aberrant splicing is frequently observed in cancer. Mutations in the splicing factor SF3B1 are particularly common in patients with chronic lymphocytic leukemia (CLL) and myelodysplastic syndromes (MDS), with different survival prognoses. We applied long-read sequencing for the investigation of the SF3B1 mutation effect on the transcriptome of MDS and CLL patients, as well as isogenic cell lines. Our results revealed that SF3B1 mutation effect was common across the different diseases and specifically altered the usage of 3’ alternative splice sites within short proximity to the canonical splice sites. Based on computational simulations, the most common K700E mutation led to destabilization of the SF3B1-mRNA binding. Furthermore, we combined the full isoform information with genome-wide SF3B1-RNA binding maps to predict the functional consequences of the aberrant splicing and gain mechanistic insights into the role of mutated SF3B1 in splicing.

2024-08-19 | GSE247658 | 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