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NONO knockdown RNA-seq and neuroblastoma PARCLIP analysis of NONO

ABSTRACT: NONO knockdown RNA-seq and neuroblastoma PARCLIP analysis of NONO

PROVIDER: PRJNA471190 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7159920.fastq.gz	Fastqsanger.gz
	SRR7159921.fastq.gz	Fastqsanger.gz
	SRR7159912.fastq.gz	Fastqsanger.gz
	SRR7159922.fastq.gz	Fastqsanger.gz
	SRR7159913.fastq.gz	Fastqsanger.gz

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NONO knockdown RNA-seq and neuroblastoma PARCLIP analysis of NONO

Project description:siRNA knockdown of NONO mRNA followed by RNA-seq was carried out in the KELLY neuroblasotma cell line. In order to determine potential regulatory targets of NONO protein, we performed differential expression analysis. To identify the RNA targets of NONO in neuroblastoma, we carried out PAR-CLIP (Photoactivatable Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation) using an antibody recognising NONO protein.

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PARCLIP analysis of NONO and SFPQ from U2OS and Hela cells

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PARCLIP analysis of NONO and SFPQ from U2OS and Hela cells

Project description:PARCLIP analysis of NONO and SFPQ from U2OS and Hela cells

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RNA binding properties of NONO and NONO-delta-ER in testis;

Project description:To investigate the RNA binding proterties of NONO and NONO-delta-ER in testis; we collected adult NONO and NONO-delta-ER mice testis We then performed eCLIP-seq respectively and convey subsequent bioinformatic analysis.

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Next Generation Sequencing Quantitative Analysis of Wild Type and NONO Knock Down Glioblastoma Cell Line(U251) Transcriptomes

Project description:We identified non-POU domain-containing octamer-binding protein (NONO), a Drosophila behavior human splicing (DBHS) protein, among the most upregulated mRNA splicing factors in glioblastoma multiforme (GBM). NONO was associated with poor prognosis in GBM patients, and overexpression of NONO promoted GBM cell proliferation, invasion and tumorigenesis in a GBM orthotopic xenograft model. Through RNA sequencing based transcriptomic profiling, we found that knockdown of NONO resulted in global changes in alternative splicing-intron retention, and identified GPX1 and CCN1 as two pre-mRNAs targeted by NONO. NONO directly bound to the intron of GPX1 pre-mRNA through the RNA-recognition motifs 2 (RRM2) domain and required interaction with another DBHS protein family member, PSPC1. Knockdown of NONO interfered with redox homeostasis in cells, at least partially, through abnormal splicing of GPX1. Finally, Auranofin, a small-molecule inhibitor targeting NONO, inhibited GBM growth in an orthotopic xenograft model in mice. Taken together, our data revealed that NONO was a key regulator of mRNA splicing in GBM, and that targeting NONO represents a novel and effective therapeutic strategy for the treatment of GBM.

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Next Generation Sequencing Quantitative Analysis of Wild Type and NONO Knock Down Glioblastoma Cell Line (GSC P3) Transcriptomes

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NONO mutations cause syndromic intellectual disability and inhibitory synaptic defects

Project description:Identifying causes of sporadic intellectual disability remains a considerable medical challenge. Here, we demonstrate that null mutations in the NONO gene, a member of the Drosophila Behavior Human Splicing (DBHS) protein family, are a novel cause of X-linked syndromic intellectual disability. Comparing humans to Nono-deficient mice revealed related behavioral and craniofacial anomalies, as well as global transcriptional dysregulation. Nono-deficient mice also showed deregulation of a large number of synaptic transcripts, causing a disorganization of inhibitory synapses, with impaired postsynaptic scaffolding of gephyrin. Alteration of gephyrin clustering could be rescued by over-expression of Gabra2 in NONO-compromised neurons. These findings link NONO to intellectual disability and first highlight the key role of DBHS proteins in functional organization of GABAergic synapses.

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NONO mutations cause syndromic intellectual disability and inhibitory synaptic defects

2015-09-02 | E-MTAB-2894 | biostudies-arrayexpress

Analysis of RNA-binding protein PSF- and NONO-associated transcripts in breast cancer

Project description:To examine the role of PSF and NONO in breast cancer cells, PSF- and NONO- associated transcripts were co-immunoprecipitated with PSF and NONO antibodies, respectively. Purified RNAs were analyzed with NGS.

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Project description:A large swath of the human proteome is dedicated to mRNA homeostasis, but most RNA-binding proteins lack chemical probes1,2. Here, we report the discovery through phenotypic screening of electrophilic small molecules that swiftly (within 4 h) and stereospecifically decrease transcripts encoding the androgen receptor (AR) and its major V7 splice variant in human prostate cancer cells. We show by chemical proteomics that these compounds covalently engage cysteine-145 on the RNA-binding protein NONO. Broader profiling revealed that covalent NONO ligands suppress a discrete set of transcripts and proteins, including multiple oncogenic transcription factors, and impair the proliferation of cancer cells. These effects were not observed following genetic disruption of NONO, which instead blocked ligand activity. The covalent ligands promote accumulation of NONO in nuclear foci and at the first 5’ splice site of immature transcripts, pointing to a trapping mechanism that may prevent compensatory action by the related protein PSPC1, which was found to increase in cancer cells following genetic or chemical perturbation of NONO. These findings, taken together, designate NONO as a druggable RNA-binding protein that can be co-opted by covalent small molecules to suppress pro-tumorigenic transcriptional networks.

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