Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA789164 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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.

2022-08-03 | GSE190950 | GEO

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

2022-08-03 | GSE191021 | GEO

Single and double knock-down of ETV6 and NFKB1 in U251 glioblastoma cell line.

Project description:To elucidate the mechanism(s) underlying the synergistic interaction between ETV6 and NFKB1, we analyzed the genome-wide transcriptional consequences of single and double knock-downs of the two TFs in U251 cells.

2016-09-26 | GSE75003 | GEO

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

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

| PRJNA789388 | ENA

FGFR3 knock-down

Project description:FGFR3 knock-down

| PRJNA330963 | ENA

SPARC knock down

Project description:SPARC knock down

| PRJNA327124 | ENA

TRIM25 promotes glioblastoma cell growth and invasion via regulation of the PRMT1/c-MYC pathway by targeting the splicing factor NONO

Project description:Ubiquitination plays an important role in proliferating and invasive characteristic of glioblastoma (GBM), similar to many other cancers. Tripartite motif 25 (TRIM25) is a member of the TRIM family of proteins, which are involved in tumorigenesis through substrate ubiquitination. Here, we found TRIM25 is upregulated in GBM and promotes glioblastoma cell growth and invasion, both in vitro and in vivo. Subsequently, we screened a panel of proteins that interact with TRIM25; mass spectrometry and co-immunoprecipitation showed that NONO was a potential substrate of TRIM25. TRIM25 knockdown reduced the K63-linked ubiquitination of NONO, which suppressed the splicing function of NONO. The dysfunctional NONO further leads to the retention of the second intron in the pre-mRNA of PRMT1 and inhibit the activation of the PRMT1/c-MYC pathway. In summary, we demonstrated that TRIM25 promotes glioblastoma cell growth and invasion by regulating the PRMT1/c-MYC pathway through mediation of the splicing factor NONO. Efforts to target the E3 ligase activity of TRIM25 or the complex interactions between TRIM25 and NONO may be useful in the treatment of GBM.

2023-07-11 | GSE236661 | GEO

Development of gene expression signatures for glioblastoma with circ2082 knock-down (KD)

Project description:Development of gene expression signatures for glioblastoma with circ2082 knock-down (KD)

| PRJNA610582 | ENA

Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 to intronic and intergenic sequences

Project description:Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53R273H in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53R273H targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin. For the study of the consequences of mutant p53 (R273H) knockdown on gene expression, total RNA from parental U251 glioblastoma cells and UsiA12 clone was prepared from two independent cell culture experiments (biological replicates) and processed for microarray-based profiling of gene expression. UsiA12 clone was derived from the U251 cells transfected with the pSuper-p53 and pCI-neo vectors.

2010-06-24 | E-GEOD-13991 | biostudies-arrayexpress

CRISPR/Cas9 knock down line

Project description:CRISPR/Cas9 knock down line

| PRJNA521684 | ENA