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

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE180848 | GEO | 2022/06/09

REPOSITORIES: GEO

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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.

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

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

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

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

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

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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

Widespread intronic polyadenylation diversifies immune cell transcriptomes

Project description:Alternative cleavage and polyadenylation (ApA) can generate mRNA isoforms with differences in 3'UTR length without changing the coding region (CDR). However, ApA can also recognize intronic polyadenylation (IpA) signals to generate transcripts that lose part or all of the CDR. We analyzed 46 3'-seq and RNA-seq profiles from normal human tissues, primary immune cells, and multiple myeloma (MM) samples and created an atlas of 4,927 high confidence IpA events represented in these cell types. Up to 16% of expressed genes in immune cells generate IpA isoforms, a majority of which are differentially used during B cell development or in different cellular environments, while MM cells display a striking loss of IpA isoforms expressed in plasma cells (PCs), their cell type of origin. IpA events can lead to truncated proteins lacking C-terminal functional domains. This can mimic ectodomain shedding through loss of transmembrane domains or alter the binding specificity of proteins with DNA-binding or protein-protein interaction domains, thus contributing to diversification of the transcriptome. In MM, loss of expression of PC IpA isoforms is associated with shorter progression-free survival and impacts key genes in MM biology and response to the therapeutic lenalidomide, including those encoding the transcription factor IKZF1 and core E3 ubiquitin ligase complex component CUL4A.

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