Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effects of FZR1 knockout on gene expression of breast tumor cells treated with cisplatin

ABSTRACT: Effects of FZR1 knockout on gene expression of breast tumor cells treated with cisplatin

PROVIDER: PRJNA597321 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10759431.fastq.gz	Fastqsanger.gz
	SRR10759432.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

Effects of FZR1 knockout on gene expression of breast tumor cells treated with cisplatin

Project description:We knockout FZR1 in T-47D breast cancer cell line, and treated the knockout and WT cells with cisplatin. The mRNA profiles were analyze.

2020-10-05 | GSE142525 | GEO

Effects of fzr1 knockdown on senescence-associated gene expression in human diploid fibroblasts.

Project description:Analysis of gene expression profile in Ras-induced senescent human diploid fibroblasts with or without depletion of fzr1/cdh1. Results provide insight into the effect on fzr1/cdh1 on the regulation of senescence-associated gene expression in human diploid fibroblasts. IMR-90-ER:Ras cells were cultured for 6 days with or without 4-hydroxytamoxifen (OHT) and were subsequently subjected to transfection with siRNA oligos against fzr1/cdh1 or control for three times (at 2 day intervals). Total RNA was isolated using Trizol reagent and were analyzed using the human 3D-Gene DNA chip (Toray) which that contains 25000 genes. The genome wide transcriptional response of proliferating cells (IMR si control2) and fzr1/cdh1 depleted senescent cells (IMR+OHT si cdh1) were compared to that of senescent cells (IMR+OHT si control).

2012-07-31 | E-GEOD-30790 | biostudies-arrayexpress

Effects of fzr1 knockdown on senescence-associated gene expression in human diploid fibroblasts.

2012-08-01 | GSE30790 | GEO

N6-methyladenosine modification of FZR1 mRNA promotes gemcitabine resistance in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) is the most lethal cancer with limited therapeutic options, and gemcitabine insensitivity remains a major challenge. N6-methyladenosine (m6A) is a prevalent nucleotide modification in mRNA that has been linked to various biological processes in human diseases, yet its role in drug sensitivity of cancer remains largely unknown. Herein, by detecting the global m6A profile in a panel of gemcitabine-sensitive and gemcitabine-insensitive PDAC cells, we identified the key role of hyper-m6A modification of the master G0/G1 regulator Fizzy and Cell Division Cycle 20 Related 1 (FZR1) in regulating gemcitabine sensitivity. Targeting m6A modification of FZR1 improves the gemcitabine treatment response of gemcitabine-insensitive PDAC cells in vitro and in vivo. Mechanistically, Gem Nuclear Organelle Associated Protein 5 (GEMIN5) was identified as a novel m6A mediator that specifically binds to m6A-modified FZR1 and recruits the eIF3 translation initiation complex to accelerate FZR1 translation. Upregulation of FZR1 maintains the G0/G1 quiescent state and impairs gemcitabine sensitivity of PDAC cells. Further clinical analysis showed that both high levels of FZR1 m6A modification and FZR1 protein indicated a poor response to gemcitabine. These findings unveil the critical function for m6A modification in regulating gemcitabine sensitivity in PDAC and identify the m6A-FZR1 axis as a potential target to enhance gemcitabine response.

2023-06-08 | GSE206969 | GEO

N6-methyladenosine-enhanced FZR1 translation contributes to gemcitabine insensitivity in pancreatic cancer via quiescence maintenance [m6A-seq]

Project description:Herein, by detecting the global m6A profile in a panel of gemcitabine-sensitive and gemcitabine-insensitive PDAC cells, we identified the key role of hyper-m6A modification of the master G0/G1 regulator Fizzy and Cell Division Cycle 20 Related 1 (FZR1) in regulating gemcitabine sensitivity. Targeting m6A modification of FZR1 improves the gemcitabine treatment response of gemcitabine-insensitive PDAC cells in vitro and in vivo. Mechanistically, Gem Nuclear Organelle Associated Protein 5 (GEMIN5) was identified as a novel m6A mediator that specifically binds to m6A-modified FZR1 and recruits the eIF3 translation initiation complex to accelerate FZR1 translation. Upregulation of FZR1 maintains the G0/G1 quiescent state and impairs gemcitabine sensitivity of PDAC cells. Further clinical analysis showed that both high levels of FZR1 m6A modification and FZR1 protein indicated a poor response to gemcitabine.

2023-06-09 | GSE206968 | GEO

N6-methyladenosine-enhanced FZR1 translation contributes to gemcitabine insensitivity in pancreatic cancer via quiescence maintenance [PAR-CLIP-Seq]

2023-06-09 | GSE206967 | GEO

The Fzr1-mediated early embryo stress response impairs fetal growth and metabolic reprogramming of offspring

Project description:Stressors during early embryogenesis influence embryo developmental trajectories and have long-term metabolic effect on offspring, but the underlying mechanism remains elusive. We performed RNA-Seq to identify transcriptional differences among control and IVF embryos. Results revealed that DNA damage and the resulting activation of Fzr1 play a central role in early embryo stress responses and subsequently affect metabolic reprogramming in offspring. To investigate the underlying molecular mechanism by which Fzr1 affected embryo development and adult metabolism. We performed RNA-Seq and H3K9me3 ChIP-seq experiments to identify transcriptional and histone modification differences among control and Fzr1-OE blastocysts. To explore the underlying mechanisms of Fzr1 activation-induced metabolic disorder, we performed RNA-Seq on the subcutaneous fat tissues of 4-month-old control and Fzr1-OE mice. We further performed reduced-representation bisulfite sequencing (RRBS) of subcutaneous fat tissues to identify possible DNA methylation alterations that could potentially mediate the intergenerational transmission of the obesity phenotype. Our findings therefore provide a new perspective on the mechanisms underlying transgenerational metabolic reprogramming and will help improve offspring health.

2023-12-31 | GSE182567 | GEO

Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney_Tumor]

Project description:Cisplatin is a potent chemotherapeutic drug, widely used in the treatment of various solid cancers. However, its clinical effectiveness is strongly limited by frequent severe adverse effects, such as nephrotoxicity and chemotherapy-induced peripheral neuropathy. Therefore, there is an urgent medical need to identify novel strategies that would limit cisplatin-induced toxicity. In the present study, we provide evidence that the FDA-approved adenosine A2A receptor antagonist istradefylline (KW6002) significantly protects from cisplatin-induced nephrotoxicity and neuropathic pain in experimental models of acute and sub-chronic cisplatin intoxication. Importantly, we also demonstrate that the anti-tumoral properties of cisplatin were not altered by istradefylline in tumor-bearing mice and even potentiated at the molecular level. Altogether, the present results support the use of istradefylline as a new valuable preventive approach for the clinical management of patients undergoing cisplatin treatment.

2022-09-12 | GSE179246 | GEO

Istradefylline (KW6002) protects from cisplatin-induced nephrotoxicity and peripheral neuropathy while preserving cisplatin anti-tumor effects [Kidney]

2022-09-12 | GSE179245 | GEO

Tumor expression data from neoadjuvant trial of cisplatin monotherapy in triple negative breast cancer patients

Project description:Evidence suggests that BRCA1 mutation associated tumors have increased sensitivity to DNA damaging agents like cisplatin. Sporadic triple negative breast cancers (TNBC) have many phenotypic similarities to BRCA1 tumors and may have a similar sensitivity to cisplatin. We tested the efficacy of cisplatin monotherapy in 28 TNBC patients in a single arm neoadjuvant trial with outcome measured by pathologic treatment response quantified using the Miller-Payne scale. We used microarrays gene expression profiles to determine tumor subtype of each trial tumor sample and to test various expression signatures for association with pathologic response to cisplatin. Pretreatment tumor samples from the clinical trial (N=24 with adequate tissue) were used for RNA extraction, linear amplification, biotin labeling and hybridization to Affymetrix U133 plus 2.0 arrays. A reference set of 51 primary breast tumors representing all subtypes of breast cancer were processed in a similar manner to include linear amplification, and hybridized to Affymetrix arrays.

2009-11-04 | E-GEOD-18864 | biostudies-arrayexpress

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