The Role of the RNA-binding protein HuR in MPNST growth and metastasis [ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA494144 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7945670.fastq.gz | Fastqsanger.gz | |||
| SRR7945680.fastq.gz | Fastqsanger.gz | |||
| SRR7945690.fastq.gz | Fastqsanger.gz | |||
| SRR7945700.fastq.gz | Fastqsanger.gz | |||
| SRR7945671.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 40 |
Similar Datasets
Project description:Oncogenic gene expression programs are essential for the development and maintenance of the cancer phenotype. An emerging view is that cancer cells can develop a strong addiction to discrete molecular regulators that control these aberrant transcription programs, making these attractive targets for effective and enduring therapies. Here, we identify the RNA-binding protein HuR as a central oncogenic driver for Malignant peripheral nerve sheath tumours (MPNSTs), which are highly aggressive sarcomas that originate from cells of the Schwann cell lineage. These neoplasms are strongly metastatic, resistant to radio-and chemotherapy and are typically fatal with no effective treatment. We find that HuR is highly elevated and binds to a multitude of cancer-associated transcripts in human MPNST samples. HuR inhibition has potent cytostatic and cytotoxic effects on tumour growth, and strongly supresses their metastatic capacity in vivo. Importantly, we find that the profound anti-tumorigenic effects of HuR stems from its unique ability to regulate multiple key oncogenic signals that ultimately converge on highly intricate transcription regulatory networks that coordinate the core biological capabilities of MPNST cells. The exceptional dependency on HuR thus confers a competitive advantage to MPNST cells for their survival, proliferation and dissemination, representing an ideal target that could be exploited for MPNST treatment.
2021-09-28 | GSE120686 | GEO
Project description:Oncogenic gene expression programs are essential for the development and maintenance of the cancer phenotype. An emerging view is that cancer cells can develop a strong addiction to discrete molecular regulators that control these aberrant transcription programs, making these attractive targets for effective and enduring therapies. Here, we identify the RNA-binding protein HuR as a central oncogenic driver for Malignant peripheral nerve sheath tumours (MPNSTs), which are highly aggressive sarcomas that originate from cells of the Schwann cell lineage. These neoplasms are strongly metastatic, resistant to radio-and chemotherapy and are typically fatal with no effective treatment. We find that HuR is highly elevated and binds to a multitude of cancer-associated transcripts in human MPNST samples. HuR inhibition has potent cytostatic and cytotoxic effects on tumour growth, and strongly supresses their metastatic capacity in vivo. Importantly, we find that the profound anti-tumorigenic effects of HuR stems from its unique ability to regulate multiple key oncogenic signals that ultimately converge on highly intricate transcription regulatory networks that coordinate the core biological capabilities of MPNST cells. The exceptional dependency on HuR thus confers a competitive advantage to MPNST cells for their survival, proliferation and dissemination, representing an ideal target that could be exploited for MPNST treatment.
2021-09-28 | GSE120685 | GEO
Project description:Oncogenic gene expression programs are essential for the development and maintenance of the cancer phenotype. An emerging view is that cancer cells can develop a strong addiction to discrete molecular regulators that control these aberrant transcription programs, making these attractive targets for effective and enduring therapies. Here, we identify the RNA-binding protein HuR as a central oncogenic driver for Malignant peripheral nerve sheath tumours (MPNSTs), which are highly aggressive sarcomas that originate from cells of the Schwann cell lineage. These neoplasms are strongly metastatic, resistant to radio-and chemotherapy and are typically fatal with no effective treatment. We find that HuR is highly elevated and binds to a multitude of cancer-associated transcripts in human MPNST samples. HuR inhibition has potent cytostatic and cytotoxic effects on tumour growth, and strongly supresses their metastatic capacity in vivo. Importantly, we find that the profound anti-tumorigenic effects of HuR stems from its unique ability to regulate multiple key oncogenic signals that ultimately converge on highly intricate transcription regulatory networks that coordinate the core biological capabilities of MPNST cells. The exceptional dependency on HuR thus confers a competitive advantage to MPNST cells for their survival, proliferation and dissemination, representing an ideal target that could be exploited for MPNST treatment.
2021-09-28 | GSE120684 | GEO
Project description:The Role of the RNA-binding protein HuR in MPNST growth and metastasis
| PRJNA494101 | ENA
Project description:The Role of the RNA-binding protein HuR in MPNST growth and metastasis [RIP-chip]
| PRJNA494145 | ENA
Project description:The Role of the RNA-binding protein HuR in MPNST growth and metastasis [RNA-seq]
| PRJNA494146 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-09-28 | GSE120687 | GEO
Project description:The effect of HuR silencing in breast epithelial cells
2010-12-14 | E-MEXP-3035 | biostudies-arrayexpress
Project description:HuR is known to regulate mRNA stability and translatability in cytoplasm. In several human tumors, the level of HuR expression has been shown to correlate with poor disease outcome. In meningioma, however, the prognostic value and the potential pro-oncogenic properties of HuR remain obscure. To clarify these, transcriptome-wide analyses in IOMM-Lee cells were performed to pinpoint the detailed molecular consequences of HuR knockdown. In IOMM-Lee cells, transcriptomic analyses revealed that HuR knockdown deregulated the signaling pathway of HIF1A and upregulated the expression of genes for cytoplasmic mRNA processing body assembly, poly(A)-specific ribonuclease activity, positive regulation of apoptosis, negative regulation of RNA splicing, global genome nucleotide-excision repair, and positive regulation of cell cycle arrest. Interestingly, HuR knockdown under hypoxic culture condition potentiated further the effects of HuR knockdown on cell growth, apoptosis, and HIF1A expression.
2017-05-11 | GSE95212 | GEO
Project description:HuR is a regulator of mRNA turnover or translation of inflammatory genes through binding to adenylate-uridylate-rich elements (ARE) and related motifs present in the 3’untranslated region (UTR) of mRNAs. We aimed to identify HuR targets in the human airway epithelial cell line BEAS-2B challenged with TNFa plus IFNg, a strong stimulus for inflammatory epithelial responses. Ribonucleoprotein (RNP) complexes from resting and cytokine-treated cells were immunoprecipitated (IP) using anti-HuR and isotype-control antibody, and eluted mRNAs were reverse-transcribed and hybridized to an inflammatory-focused gene array. The chemokines CCL2, CCL8, CXCL1 and CXCL2 ranked highest among 27 signaling and inflammatory genes significantly enriched in the HuR RNP-IP from stimulated cells over the control IP. Among these, 20 displayed published HuR binding motifs. Association of HuR with the four endogenous chemokine mRNAs was validated by single-gene RNP-IP, and shown to be 3’UTR-dependent by biotin pull-down assay. Cytokine treatment increased mRNA stability only for CCL2 and CCL8, and transient silencing and overexpression of HuR affected only CCL2 and CCL8 expression in primary and transformed epithelial cells. Cytokine-induced CCL2 mRNA was predominantly cytoplasmic; conversely, CXCL1 mRNA remained mostly nuclear and unaffected, as CXCL2, by changes in HuR levels. Increase in cytoplasmic HuR and HuR target expression partially relied on the inhibition of AMP-dependent kinase, a negative regulator of HuR nucleocytoplasmic shuttling. We postulate that HuR critically regulates the epithelial response, by associating with multiple adenylate-uridylate-rich elements (ARE)-bearing, functionally related inflammatory transcripts. On the basis of genome-wide studies probing the relationship between RNA-binding proteins and the functional profile of their associated transcripts, we combined the specific HuR immunoprecipitation of RNPs and the genome-scale microarray to profile the target mRNAs of HuR in the human airway epithelial cell line BEAS-2B challenged with very strong inflammatory stimulation, TNFa plus IFNG. The array platform we used is the Human Autoimmune and Inflammatory Response Gene Array (SuperArray Bioscience, Frederick, MD). To validate the association of HuR and its target mRNAs, we planned to apply biotin pull-down assay. HuR overexpression and knockdown assays were also planned to further verify the association of HuR and its target mRNAs. Overall, we did three biological replicates for the IP array experiments, which include both IgG1 control IP and HuR IP arrays.
2010-11-10 | E-GEOD-25264 | biostudies-arrayexpress