Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SF3B1 inhibitor pladienolide B induces pyroptosis of ovarian cancer cells

ABSTRACT: SF3B1 inhibitor pladienolide B induces pyroptosis of ovarian cancer cells

PROVIDER: PRJNA918583 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22984590_1.fastq.gz	Fastqsanger.gz
	SRR22984590_2.fastq.gz	Fastqsanger.gz
	SRR22984591_1.fastq.gz	Fastqsanger.gz
	SRR22984591_2.fastq.gz	Fastqsanger.gz
	SRR22984592_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

SF3B1 inhibitor pladienolide B induces pyroptosis of ovarian cancer cells

Project description:In order to explore the effect of SF3B1 inhibitor, pladienolide B, on ovarian cancer cells, OVCAR8 cells were treated with DMSO or 2nM pladienolide B for 72h. Cells were collected and performed RNA sequencing.

2023-11-25 | GSE222199 | GEO

Citric acid, an ovarian cancer metabolite, induces pyroptosis via caspase-4/TXNIP-NLRP3-GSDMD pathway in ovarian cancer

Project description:Malignant tumors display profound changes in cellular metabolism, yet how these altered metabolites affect the development and growth of tumors is not fully understood. Here, we used metabolomics to analyze the metabolic profile differences in ovarian cancer, and found that citric acid (CA) is the most significantly downregulated metabolite. Recently, CA has been reported to inhibit the growth of a variety of tumor cells, but whether it is involved in pyroptosis of ovarian cancer and its potential molecular mechanisms still remains to be further investigated. Here, we demonstrated that CA inhibits the growth of ovarian cancer cells in a dose-dependent manner. RNA-seq analysis revealed that CA significantly promoted the expression of thioredoxin interacting protein (TXNIP) and caspase-4 (CASP4). Morphologic examination by transmission electron microscopy indicated that CA-treated ovarian cancer cells exhibited typical pyroptosis characteristics. Further mechanistic analyses showed that CA facilitates pyroptosis via CASP4/TXNIP-NLRP3-Gesdermin-d (GSDMD) pathway in ovarian cancer. This study elucidated that CA induces ovarian cancer cell death through classical and non-classical pyroptosis pathways, which may be beneficial as an ovarian cancer therapy.

2022-08-01 | GSE189851 | GEO

Nur77 induces GSDMC-mediated pyroptosis

Project description:Pyroptosis is a type of lytic cell death executed by members of the gasdermin family. It has been demonstrated that induction of pyroptosis can effectively inhibit tumor growth, which implicates a new strategy for clinical tumor therapy, especially for those tumors (such as melanoma) that are insensitive or resistant to the induction of apoptosis.By means of a chemical compound DBIC, designed and identified by our group recently, to induce GSDMC-mediated pyroptosis in melanoma cells.

2025-07-07 | GSE273365 | GEO

Regulation of pyroptosis in radiation induces mouse intestine cells

Project description:Pyroptosis is a recently discovered form of lytic cell death that is characterized by cell swelling and formation of pores and large bubbles on the plasma membrane. We find radiation could induce pyroptosis in human colorectal cancer HCT116 cells, and irradiation induces pyroptosis in mouse normal intestine MODEK cells only after 36 hours and over 8.0 Gy. In view of the significant pyroptosis effect of MODE-K cells, we selected 4Gy and 12Gy, 24h and 48h for experiments. After ONT full-length transcriptome sequencing, the cell pyroptosis model can screen out the differential genes related to cell pyroptosis, which is helpful to further explore the mechanism of pyroptosis of MODE-K cells.

2024-08-01 | GSE211709 | GEO

SF3B1 Degron knockdown RNA-seq

Project description:Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.

2015-03-11 | E-GEOD-66719 | biostudies-arrayexpress

SF3B1

Project description:SF3B1

| PRJNA848802 | ENA

Nur77 induces GSDMC-mediated pyroptosis

Project description:Nur77 induces GSDMC-mediated pyroptosis

| PRJNA1141494 | ENA

Citric acid, an ovarian cancer metabolite, induces pyroptosis via caspase-4/TXNIP-NLRP3-GSDMD pathway in ovarian cancer

Project description:Citric acid, an ovarian cancer metabolite, induces pyroptosis via caspase-4/TXNIP-NLRP3-GSDMD pathway in ovarian cancer

| PRJNA784786 | ENA

SF3B1 association with chromatin determines splicing outcomes

Project description:Much remains unknown concerning the mechanism by which the splicing machinery pinpoints short exons within intronic sequences and how splicing factors are directed to their pre-mRNA targets. Part of the explanation probably lies in differences in chromatin organization between exons and introns. Proteomic, co-immunoprecipitation, and sedimentation analyses described here indicated that SF3B1, an essential splicing component of the U2 snRNP complex, is strongly associated with nucleosomes. ChIP-seq and RNA-seq analyses revealed that SF3B1 is specifically bound to nucleosomes located at exonic positions. SF3B1 binding is enriched at nucleosomes positioned over short exons flanked by long introns that are also characterized by differential GC content between exons and introns. Disruption of SF3B1 binding to such nucleosomes affected the splicing of these exons similarly to inhibition of SF3B1 expression. Our findings suggest that the association of SF3B1 with nucleosomes is functionally important for splice site recognition and that SF3B1 conveys splicing-relevant information embedded in chromatin structure. MNase-seq on Input and SF3B1 pull-down, mRNA-seq on control and SF3B1 si-RNA treated cells as well as on TSA (Trichostatin A) treated and untreated cells.

2015-04-22 | E-GEOD-65644 | biostudies-arrayexpress

Thioridazine induces pyrolysis and autophagy in epithelial ovarian cancer

Project description:Thioridazine exhibits inhibitory effects on various tumors, including epithelial ovarian cancer, but the mechanisms remain unclear. Proliferation and invasion were assessed using CCK8 and Matrigel invasion assays. Autophagy and pyroptosis-related markers were detected via Western blot. Autophagy flux was tracked using the mRFP-GFP-LC3 reporter. Autophagy inhibitors 3MA andBufA1 were used to confirm whether autophagy flux was functioning properly. RNA sequencing was performed to identify differentially expressed genes, and Co-IP was used to detect interacting proteins. A subcutaneous tumorigenesis experiment in nude mice was conducted to evaluate the effect of thioridazine in vivo. As a result, thioridazine inhibited proliferation and invasion of EOC while promoting autophagy and pyroptosis. The upregulation of the pyroptosis marker NLRP3 may be attributed to DRD2 inhibition. Inhibition of autophagy enhanced NLRP3 expression, and the autophagy inhibitor CQ increased the tumor-inhibiting effects of thioridazine. In conclusion, thioridazine inhibited EOC proliferation and invasion by inducing pyroptosis and autophagy, with autophagy playing a protective role in thioridazine treatment. Thioridazine combined with the autophagy inhibitor CQ may be an effective treatment for EOC.

2025-04-24 | GSE295565 | 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