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Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [CLIP-seq]

ABSTRACT: Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [CLIP-seq]

PROVIDER: PRJNA749773 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15249968.fastq.gz	Fastqsanger.gz
	SRR15249969.fastq.gz	Fastqsanger.gz
	SRR15249970.fastq.gz	Fastqsanger.gz
	SRR15249971.fastq.gz	Fastqsanger.gz
	SRR15249972.fastq.gz	Fastqsanger.gz

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Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [3-seq]

Project description:We explored the regulation of intronic polyadenylation (IPA) isoforms by doxorubicin and HuR in several subcellular compartments.

2022-06-09 | GSE180847 | GEO

Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [CLIP-seq]

Project description:We investigated the regulation by doxorubicin of HuR binding to RNA near intronic polyadenylation (IPA) sites in several subcellular compartments of breast cancer cells.

2022-06-09 | GSE180848 | GEO

Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [total RNA-seq]

Project description:We explored the regulation of intronic polyadenylation (IPA) isoforms by doxorubicin and HuR in breast cancer cells.

2022-06-09 | GSE180849 | GEO

Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin

Project description:Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin

| PRJNA749765 | ENA

Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [3-seq]

Project description:Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [3-seq]

| PRJNA749772 | ENA

Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [total RNA-seq]

Project description:Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin [total RNA-seq]

| PRJNA749775 | ENA

Compartment-specific and HuR-coordinated regulation of intronic polyadenylation isoforms by doxorubicin

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-06-09 | GSE180850 | GEO

Compartment-specific and ELAVL1-coordinated regulation of intronic polyadenylation isoforms by doxorubicin.

Project description:Intronic polyadenylation (IPA) isoforms, which contain alternative last exons, are widely regulated in various biological processes and by many factors. However, little is known about their cytoplasmic regulation and translational status. In this study, we provide the first evidence that the genome-wide patterns of IPA isoform regulation during a biological process can be very distinct between the transcriptome and translatome, and between the nucleus and cytosol. Indeed, by 3'-seq analyses on breast cancer cells, we show that the genotoxic anticancer drug, doxorubicin, preferentially down-regulates the IPA to the last-exon (IPA:LE) isoform ratio in whole cells (as previously reported) but preferentially up-regulates it in polysomes. We further show that in nuclei, doxorubicin almost exclusively down-regulates the IPA:LE ratio, whereas in the cytosol, it preferentially up-regulates the isoform ratio, as in polysomes. Then, focusing on IPA isoforms that are up-regulated by doxorubicin in the cytosol and highly translated (up-regulated and/or abundant in polysomes), we identify several IPA isoforms that promote cell survival to doxorubicin. Mechanistically, by using an original approach of condition- and compartment-specific CLIP-seq (CCS-iCLIP) to analyze ELAVL1-RNA interactions in the nucleus and cytosol in the presence and absence of doxorubicin, as well as 3'-seq analyses upon ELAVL1 depletion, we show that the RNA-binding protein ELAVL1 mediates both nuclear down-regulation and cytosolic up-regulation of the IPA:LE isoform ratio in distinct sets of genes in response to doxorubicin. Altogether, these findings reveal differential regulation of the IPA:LE isoform ratio across subcellular compartments during drug response and its coordination by an RNA-binding protein.

| S-EPMC9341504 | biostudies-literature

RIP-chip of HuR in MCF7 cells exposed to doxorubicin

2011-12-31 | GSE33055 | GEO

RIP-chip of HuR in MCF7 cells exposed to doxorubicin

Project description:The purpose of the study was to identify mRNA bound to HuR in the presence of doxorubicin in MCF7 cells. We collected cytoplasmic RNA from untreated and treated cells and detected differentially expressed genes (DEGs). We also coimmunoprecipitated HuR and IgG (as control) from doxorubicin treated cells. Comparison between HuR RIP and IgG RIP signals was used to discriminate specific mRNA bound to HuR. HuR coimmmunoprecipitated material was hybridized together with cytoplasmic mRNA of doxorubicin treated cells, enabling the fold enrichment calculation and the selection of mRNAs bound to HuR. Keywords: RIP-Chip, HuR, doxorubicin, MCF7, HuR consensus binding, post-transcriptional regulation. We subjected MCF7 cells to starvation for 24h and then we added doxorubicin at final concentration of 10 uM, profiling before and after 4 hours of treatment in biological quadruplicate (only on cytoplasmic mRNAs, as HuR was found in the cytoplasm). Differentially expressed genes, altered during the treatment, were identified. Data derived from HuR RIP-Chip and IgG RIP-Chip (in biological quadruplicate) allowed the identification of specific mRNAs bound to HuR. The comparison between HuR RIP-Chip and cytoplasmic extracts from doxorubicin treated cells (in biological triplicate) identified those genes that were more strictly bound to HuR independently from their expression levels.

2011-12-31 | E-GEOD-33055 | biostudies-arrayexpress

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