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

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

PROVIDER: PRJNA853162 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19857861_1.fastq.gz	Fastqsanger.gz
	SRR19857861_2.fastq.gz	Fastqsanger.gz
	SRR19857862_1.fastq.gz	Fastqsanger.gz
	SRR19857862_2.fastq.gz	Fastqsanger.gz
	SRR19857863_1.fastq.gz	Fastqsanger.gz

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N6-methyladenosine-enhanced FZR1 translation contributes to gemcitabine insensitivity in pancreatic cancer via quiescence maintenance [PAR-CLIP-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 | GSE206967 | GEO

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

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

| PRJNA853161 | ENA

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

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

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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

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

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

PAR-TERRA RNA directs homologous sex chromosome pairing

Project description:In mammals, homologous chromosomes rarely pair outside meiosis. One exception is the X chromosome, which transiently pairs during X-chromosome inactivation (XCI). How two chromosomes find each other in 3D space is not known. Here, we reveal a required interaction between the X-inactivation center (Xic) and the telomere in mouse embryonic stem (ES) cells. The subtelomeric, pseudoautosomal regions (PARs) of the two sex chromosomes (X and Y) also undergo pairing in both female and male cells. PARs transcribe a class of telomeric RNA, dubbed PAR-TERRA, which accounts for a vast majority of all TERRA transcripts. PAR-TERRA binds throughout the genome, including to the PAR and Xic. During X-chromosome pairing, PAR-TERRA anchors the Xic to the PAR, creating a ‘tetrad’ of pairwise homologous interactions (Xic–Xic, PAR–PAR, and Xic–PAR). Xic pairing occurs within the tetrad. Depleting PAR-TERRA abrogates pairing and blocks initiation of XCI, whereas autosomal PAR-TERRA induces ectopic pairing. We propose a ‘constrained diffusion model’ in which PAR-TERRA creates an interaction hub to guide Xic homology searching during XCI.

2017-07-10 | GSE69887 | GEO

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