Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Effect of USP1 knockout on gene expression in bladder cancer cells

PROVIDER: PRJNA970255 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24464847_1.fastq.gz	Fastqsanger.gz
	SRR24464847_2.fastq.gz	Fastqsanger.gz
	SRR24464848_1.fastq.gz	Fastqsanger.gz
	SRR24464848_2.fastq.gz	Fastqsanger.gz
	SRR24464849_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Analysis of the role of SMARCB1 in bladder cancer cell line T24 [ATAC-seq]

Project description:To identify DNA accessibility targets regulated by the SWI/SNF subunit SMARCB1 in bladder cancer, we compared the ATAC-seq signals in T24 cells engineered for SMARCB1 knockout, non-targeting control, or SMARCB1 re-expression following knockout. Analysis of altered DNA accessibility profiles revealed new roles for SMARCB1 in the regulation of gene expression in bladder cancer, and suggested new therapeutic opportunities.

2023-11-17 | GSE213964 | GEO

The deubiquitinase cofactor UAF1 interacts with USP1 and plays an essential role in spermiogenesis

Project description:Spermiogenesis defines the final phase of male germ cell differentiation. Multiple deubiquitinating enzymes have been linked to spermiogenesis, yet the impacts of deubiquitination on spermiogenesis remain poorly characterized. Here, we investigated the function of UAF1 in mouse spermiogenesis and male fertility. We selectively deleted Uaf1 in premeiotic germ cells using Stra8-Cre knock-in mouse strain (Uaf1 sKO), and found that Uaf1 is essential for spermiogenesis and male fertility. We found that UAF1 interacts and colocalizes with USP1 in testes. Conditional knockout of Uaf1 in testes results in disturbed expression and localization of USP1, suggesting that UAF1 regulates spermiogenesis through the function of the deubiquitinating enzyme USP1. We used tandem mass tag-based proteomics to identify differentially expressed proteins and potential underlying mechanisms, and found that conditional knockout Uaf1 in testes results in reduced levels of proteins essential for spermiogenesis. Thus, the UAF1/USP1 deubiquitinase complex is essential for normal spermiogenesis by regulating the levels of spermiogenesis-related proteins.

2024-02-07 | PXD046120 | Pride

Gene expression changes in breast cancer cells upon USP1 knockdown [RNA-Seq]

Project description:To explore the function of deubiquitinase USP1 in breast cancer cells, we performed RNA sequencing to analyze the expression pattern changes by knockdown of USP1 in MCF7 cells.

2021-03-14 | GSE111838 | GEO

USP1 expression driven by EWS-FLI1 transcription factor stabilizes Survivin and promotes Ewing sarcoma cell survival

Project description:Ewing sarcoma (EWS) is a malignant pediatric bone cancer. Most Ewing sarcomas are driven by EWS-FLI1 oncogenic transcription factor that plays roles in transcriptional regulation, DNA damage response, cell cycle checkpoint control, and alternative splicing. USP1, a deubiquitylase which regulates DNA damage and replication stress responses, is overexpressed at both the mRNA and protein levels in EWS cell lines compared to human mesenchymal stem cells, the EWS cell of origin. The functional significance of high USP1 expression in Ewing sarcoma is not known. Here, we identify USP1 as a transcriptional target of EWS-FLI1 and a key regulator of EWS cell survival. We show that EWS-FLI1 knockdown decreases USP1 mRNA and protein levels. ChIP and ChIP-seq analyses show EWS-FLI1 occupancy on the USP1 promoter. Importantly, USP1 knockdown or inhibition arrests EWS cell growth and induces cell death by apoptosis. We observe destabilization of Survivin (also known as BIRC5 or IAP4) and activation of caspases-3 and -7 following USP1 knockdown or inhibition in the absence of external DNA damage stimuli. Notably, EWS cells display hypersensitivity to combinatorial treatment of doxorubicin or etoposide, EWS standard of care drugs, and USP1 inhibitor compared to single agents alone. Together, our study demonstrates that USP1 is regulated by EWS-FLI1, the USP1-Survivin axis promotes EWS cell survival, and USP1 inhibition sensitizes EWS cells to standard of care chemotherapy.

2024-01-26 | PXD041033 | Pride

Homo sapiens

Project description:Effect of increased FOXA1 on gene expression in bladder cancer cells

| PRJNA242274 | ENA

ETV5 silencing in bladder cancer cell line 97-7

Project description:We hypothesized that ETV5 may be a mediator of the oncogenic effects of mutant FGFR3 in bladder cancer cells ETV5 was silenced by shRNA in the bladder cancer cell line 97-7 to investigate effect on phenotype. To identify downstream gene targets of ETV5 we compared gene expression profiles in silenced and control cells.

2018-11-09 | GSE122306 | GEO

mTOR signaling pathway and targeting c-myc

Project description:Purpose: To investigate the tumor-promoting role of STIL in bladder cancer. Method: We established the STIL knockout cell line in which the target gene was knocked out by sgRNA. RNA was extracted from cells using trizol reagent(Invitrogen) Result: Through RNA-sequencing analysis of wild-type and STIL-deficient UMUC3 cell lines, the downstream signaling pathways that STIL may be involved in were determined. We found that the PI3K/AKT/mTOR signaling pathway and c-myc were significantly inactivated when STIL was knocked out in bladder cancer. Our RNA-sequencing analysis results showed that the downstream molecules of c-myc (MCM4, HSPD1, EIF2S2, DDX21, DDX18, CBX3, ABCE1) were significantly down-regulated in bladder cancer cells after knockout. Conclusion: STIL enhances the PI3K/AKT/mTOR pathway, which consequently upgraded the expression of c-myc, ultimately promoting the occurrence and progression of bladder cancer C. STIL may suggest potential utility for bladder cancer therapy.

2023-08-01 | GSE211756 | GEO

E-GEOD-56037

Project description:Effect of increased FOXA1 on gene expression in bladder cancer cells

2025-01-24 | E-GEOD-56037 | ExpressionAtlas

Gene expression changes in breast cancer cells upon USP1 knockdown [RNA-Seq]

Project description:Gene expression changes in breast cancer cells upon USP1 knockdown [RNA-Seq]

| PRJNA438337 | ENA

Epigenetic silencing of the dual-role signal mediator, ANGPTL4 in tumor tissue and its overexpression in the urothelial carcinoma microenvironment

Project description:To investigate the effect of ANGPTL4 expression on bladder cancer cells, expression profile was compared in BFTC 905 cells overexpressed with control vector vs human full length ANGPTL4 gene.

2017-10-01 | GSE102170 | 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