The Role of the RNA-binding protein HuR in MPNST growth and metastasis [RIP-chip]
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PROVIDER: PRJNA494145 | ENA |
REPOSITORIES: ENA
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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 | GSE120684 | 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 | GSE120685 | 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 [ChIP-seq]
| PRJNA494144 | ENA
Project description:The Role of the RNA-binding protein HuR in MPNST growth and metastasis [RNA-seq]
| PRJNA494146 | ENA
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 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: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