MRNA stability factor HuR promotes immune evasion in pancreatic ductal adenocarcinoma [RIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1212182 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32037877_1.fastq.gz | Fastqsanger.gz | |||
| SRR32037877_2.fastq.gz | Fastqsanger.gz | |||
| SRR32037878_1.fastq.gz | Fastqsanger.gz | |||
| SRR32037878_2.fastq.gz | Fastqsanger.gz | |||
| SRR32037879_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
Similar Datasets
Project description:mRNA stability factor HuR promotes immune evasion in pancreatic ductal adenocarcinoma
| PRJNA1212072 | ENA
Project description:The limited infiltration of tumor-specific T cells into the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment (TME) is hypothesized to limit immunotherapy responses. The RNA-binding protein, HuR (ELAVL1), is over-abundant in PDAC, and its expression negatively correlates with T cell infiltration. In the immunocompetent Kras-p53-Cre (KPC) model, we found HuR depletion impairs tumor growth. To investigate the impact of the immune cells on tumor growth, we analyzed the infiltrated immune population in tumors and found that HuR-depleted tumors had increased T cell infiltration and activation. Mechanistically, HuR mediated stabilization of mTOR pathway and enhanced PDAC nutrient consumption, which impaired local T-cell antitumor function. We found that HuR suppression of antitumor immunity has profound consequences, as HuR-deficient tumors are sensitive to immune checkpoint blockade, while isogenic, wildtype tumors are resistant. These findings describe a novel role of HuR in PDAC facilitating tumor immune suppression in the PDAC TME by inhibiting T cell infiltration and function.
2025-02-05 | GSE287349 | GEO
Project description:Integrative regulatory mapping indicates that the RNA-binding protein HuR (ELAVL1) couples pre-mRNA processing and mRNA stability In this dataset, we employed two distinct experiments. 1) HuR RIP-chip to identify mRNA targets of HuR. 2) HuR knockdown to identify mRNAs whose expression are dependent on HuR. All 12 samples were normalized with PLIER using Affymetrix power tools. To identify RNA targets of HuR, HuR RIP samples were compared to Mock RIP samples. To identify RNA regulated by HuR, HuR knockdown samples were compared to mock knockdown samples.
2011-08-18 | E-GEOD-29778 | biostudies-arrayexpress
Project description:The limited infiltration of tumor-specific T cells into the pancreatic ductal adenocarcinoma (PDAC) tumor microenvironment (TME) is hypothesized to limit immunotherapy responses. The RNA-binding protein, HuR (ELAVL1), is over-abundant in PDAC, and its expression negatively correlates with T cell infiltration. In the immunocompetent Kras-p53-Cre (KPC) model, we found HuR depletion impairs tumor growth. To investigate the impact of the immune cells on tumor growth, we analyzed the infiltrated immune population in tumors and found that HuR-depleted tumors had increased T cell infiltration and activation. Mechanistically, HuR mediated stabilization of mTOR pathway and enhanced PDAC nutrient consumption, which impaired local T-cell antitumor function. We found that HuR suppression of antitumor immunity has profound consequences, as HuR-deficient tumors are sensitive to immune checkpoint blockade, while isogenic, wildtype tumors are resistant. These findings describe a novel role of HuR in PDAC facilitating tumor immune suppression in the PDAC TME by inhibiting T cell infiltration and function.
2025-02-05 | GSE287307 | GEO
Project description:Integrative regulatory mapping indicates that the RNA-binding protein HuR (ELAVL1) couples pre-mRNA processing and mRNA stability In this dataset, we employed two distinct experiments. 1) HuR RIP-chip to identify mRNA targets of HuR. 2) HuR knockdown to identify mRNAs whose expression are dependent on HuR.
2011-08-19 | GSE29778 | GEO
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
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.
2011-12-31 | GSE33055 | GEO
Project description:RNA binding protein, Human Antigen R (HuR/ELAVL1), regulates mRNA stability of key species involved in pancreatic ductal adenocarcinoma (PDAC) cell survival under conditions of chemotherapeutic stress, hypoxia, low glucose environment. We used RNA immunoprecipitation-microarray or RNP-IP from cytoplasmic extracts of PDAC cell lines exposed to chemotherpaeutic stress (olaparib and gemcitabine) to evaluate whole transcriptome gene expression profile associated with HuR and find novel trargtes associated with DNA repair functions of HuR.
2022-04-20 | GSE166951 | GEO
Project description:Post-transcriptional regulatory networks are dependent on the interplay of many RNA-binding proteins having a major role in mRNA processing events in mammals. We have been interested in the concerted action of the two RNA-binding proteins hnRNP A1 and HuR, both stable components of immunoselected hnRNP complexes and having a major nuclear localization. Specifically, we present here the application of the RNA-immunoprecipitation (RIP)-Chip technology to identify a population of nuclear transcripts associated with hnRNP A1-RNPs as isolated from the nuclear extract of either HuR WT or HuR-depleted (KO) mouse embryonic fibroblast (MEF) cells. The outcome of this analysis was a list of target genes regulated via HuR for their association (either increased or reduced) with the nuclear hnRNP A1-RNP complexes. Real time PCR analysis was applied to validate a selected number of nuclear mRNA transcripts, as well as to identify pre-spliced transcripts (in addition to their mature mRNA counterpart) within the isolated nuclear hnRNP A1-RNPs. The differentially enriched mRNAs were found to belong to GO categories relevant to biological processes anticipated for hnRNP A1 and HuR (such as transport, transcription, translation, apoptosis and cell cycle) indicative of their concerted function in mRNA metabolism. Ribonucleoprotein Immunoprecipitation (RIP) using hnRNP A1 specific antibody was performed in nuclear extracts from HuR WT and HuR KO Mouse Embryonic Fibroblasts (MEFs). RNA isolated from these IPs together with nuclear RNA from the two cell types, was subjected to microarray analysis. Three biological replicates, representing three independent experiments, are available for each condition except in the case of nuclear RNA isolated from HuR WT MEFs that one replicate didn’t pass the quality control.
2013-11-01 | E-GEOD-49225 | biostudies-arrayexpress
Project description:RNA-binding proteins coordinate the fates of multiple RNAs, but the principles underlying these global interactions remain poorly understood. We elucidated regulatory mechanisms of the RNA-binding protein HuR, by integrating data from diverse high-throughput targeting technologies, specifically PAR-CLIP, RIP-chip, and whole-transcript expression profiling. The number of binding sites per transcript, degree of HuR-association, and degree of HuR-dependent RNA stabilization were positively correlated. Pre-mRNA and mature mRNA containing both intronic and 3' UTR binding sites were more highly stabilized than transcripts with only 3' UTR or only intronic binding sites, suggesting that HuR couples pre-mRNA processing with mature mRNA stability. We also observed HuR-dependent splicing changes and substantial binding of HuR in poly-pyrimidine tracts of pre-mRNAs. Comparison of the spatial patterns surrounding HuR and miRNA binding sites provided functional evidence for HuR-dependent antagonism of proximal miRNA-mediated repression. We conclude that HuR coordinates gene expression outcomes at multiple interconnected steps of RNA processing. HuR (ELAVL1) PAR-CLIP
2011-08-19 | E-GEOD-29779 | biostudies-arrayexpress