The Role of the RNA-binding protein HuR in MPNST growth and metastasis [RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA494146 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7945720.fastq.gz | Fastqsanger.gz | |||
| SRR7945721.fastq.gz | Fastqsanger.gz | |||
| SRR7945712.fastq.gz | Fastqsanger.gz | |||
| SRR7945722.fastq.gz | Fastqsanger.gz | |||
| SRR7945713.fastq.gz | Fastqsanger.gz |
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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 | 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 | 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 [ChIP-seq]
| PRJNA494144 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-09-28 | GSE120687 | GEO
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:Human antigen R (HuR) protein, a RNA binding protein (RBP), has been reported to regulate essential steps in RNA metabolism and immune response in a variety of cell types, but its function in metabolism remains unclear. This study identifies HuR as a major repressor during adipogenesis. Knockdown and overexpression of HuR in primary adipocyte culture enhances and inhibits adipogenesis in vitro, respectively. Fat-specific knockout of HuR significantly enhances adipogenic gene program in all three major adipose tissues including epidydimal, inguinal white and brown adipose tissue, accompanied with systemic glucose intolerance and insulin resistance. Conversely, transgenic overexpression of HuR in adipose tissue prevents the HFD induced obesity by repressing adipogenesis. Mechanistically, HuR may inhibit adipogenesis by recognizing and modulating the stability of hundreds of adipocyte transcripts, including the mRNA of Insig1, a negative regulator during adipogenesis. Taken together, our work establishes HuR as a novel posttranscriptional regulator of adipogenesis and provides a new insight into how RNA processing contributes to adipocyte development.
2019-09-09 | GSE124278 | GEO
Project description:We utilized three murine MPNST cell lines. 67C-4 and #5NPCIS cell lines are derived from spontaneously arising tumors in mice mutated for NF1 and p53 (so-called NP-cis mice; PMID: 12154062). SN4-4 cells originated from MPNST tumors induced by injecting adenovirus containing Cas9 and guide RNA for Nf1 and p53 into the sciatic nerves, resulting in NF1/p53-null MPNST (PMID: 32456131). We implanted 5 x 10^6 murine MPNST cells, subcutaneously, into the flanks of 6-8 weeks old gender-matched C57BL/6 mice (for 67C-4 and #5NPCIS) and BALB/c mice (for SN4-4 mice) to generate MPNST tumors. All mice were procured from Envigo. Upon reaching a size of 300-500 mm3, the mice were euthanized to harvest the tumors, which were subsequently flash frozen using liquid nitrogen and processed for RNA sequencing.
2024-06-19 | GSE244829 | GEO