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SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells I

ABSTRACT: SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells I

PROVIDER: PRJNA479751 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7472460_1.fastq.gz	Fastqsanger.gz
	SRR7472460_2.fastq.gz	Fastqsanger.gz
	SRR7472461_1.fastq.gz	Fastqsanger.gz
	SRR7472461_2.fastq.gz	Fastqsanger.gz
	SRR7472462_1.fastq.gz	Fastqsanger.gz

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SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells II

Project description:Oncoproteins such as the BRAFV600E kinase entrust cancer cells with malignant properties, but they also create unique vulnerabilies. Therapeutic targeting of the BRAFV600E-driven cytoplasmic signaling network has proven ineffective, since patients regularly relapse with reactivation of the targeted signaling pathways. Here, we identified the nuclear protein SFPQ to be synthetically lethal with BRAFV600E in a loss-of-function shRNA screen. SFPQ depletion decreased proliferation and induced apoptosis in BRAFV600E-driven colorectal and melanoma cells, and reduced tumor growth in xenografts. Mechanistically, SFPQ loss in BRAF-mutant cancer cells triggered the Chk1-dependent replication checkpoint, resulting in replication stress in the absence of overt DNA damage. Affected cells stalled in S-Phase with hallmark signs of impaired replication factories. Induction of BRAFV600E and concomitant loss of SFPQ sensitized cells to a combination of DNA replication checkpoint inhibitors and chemically induced replication stress, pointing towards future therapeutic approaches exploiting nuclear vulnerabilities induced by BRAFV600E.

2020-04-27 | GSE149370 | GEO

SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells I

2019-12-31 | GSE116631 | GEO

SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells

Project description:SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells

| PRJNA628515 | ENA

SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells II

Project description:SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells II

| PRJNA628517 | ENA

SFPQ depletion is synthetically lethal with BRAFV600E in colorectal cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-04-27 | GSE149371 | GEO

Microarray of zebrafish (Danio rerio) sfpq-/-;Tg(mnx1:GFP) against sfpq+/+;Tg(mnx1:GFP) and sfpq+/-;Tg(mnx1:GFP) siblings at 24 hpf

Project description:Phenotypic characterisation of our zebrafish sfpq homozygous mutants revealed a restricted set of specific defects, unexpected for a protein expressed ubiquitously and involved in such general mechanisms. The CNS was prominently affected, showing brain boundary and axonal defects associated with absence of motility. To investigate a possible specificity in SFPQ functional targets by microarray RNA profiling analysis, comparing the transcriptome of the sfpq homozygous mutants with its wild type and heterozygous siblings at the earliest stage at which the phenotype is robustly recognizable.

2017-09-01 | E-MTAB-5559 | biostudies-arrayexpress

SFPQ interacted proteins in HEK293T nucleus and cytoplasm

Project description:Splicing factor proline and glutamine rich (SFPQ), DNA- and RNA binding protein, is crucial in various nuclear processes, including paraspeckle formation, miRNA synthesis and specially in transcription regulation. In addition, SFPQ play a role in the innate immune response to viruses, including DNA and RNA viruses. However, the connections between SFPQ and EMCV infection remain unclear. Here we report that the SFPQ is essential for EMCV replication. Depletion of SFPQ impairs EMCV production, while forced expression of SFPQ could promote viral replication. Mechanistically, EMCV inhibited viral RNA-mediated type I IFN and IL6 production to eliminate host antiviral immune responses. Cellular SFPQ was cleaved by the EMCV proteinase then entered the cytoplasm and interacted with other ribosomal proteins to facilitate its internal ribosome entry site (IRES)-dependent translation. Moreover, loss of SFPQ may impress host translation related gene expression and thus facilitate the EMCV replication. Altogether, our work provides a possible target for resisting EMCV or EMCV-like virus’s infection.

2019-01-10 | PXD011865 | Pride

The kinase inhibitor GNF-7 is synthetically lethal in topoisomerase 1 deficient Ewing Sarcoma

Project description:The kinase inhibitor GNF-7 is synthetically lethal in topoisomerase 1 deficient Ewing Sarcoma

| PRJNA1271555 | ENA

Loss of function of CDK7 is Synthetically Lethal with Fatty Acid Oxidation Inhibition in Glioblastoma

Project description:Loss of function of CDK7 is Synthetically Lethal with Fatty Acid Oxidation Inhibition in Glioblastoma

| PRJNA956908 | ENA

Paraspeckle-Independent Co-Transcriptional Regulation of Nuclear microRNA Biogenesis by SFPQ [PRO-seq]

Project description:MicroRNAs (miRNAs) play crucial roles in physiological functions and diseases such as cancer, but the regulation of their nuclear biogenesis remains poorly understood. Here, BioID on Drosha, the catalytic subunit of the microprocessor complex, revealed its proximity to SFPQ, a multifunctional RNA-binding protein (RBP) notably involved in forming the paraspeckle nuclear condensates. SFPQ depletion impacted both primary and mature miRNA expression, while other crucial paraspeckle proteins or the paraspeckle scaffolding lncRNA NEAT1 did not, indicating a unique paraspeckle-independent role. Comprehensive transcriptomic analyses showed that SFPQ loss broadly affects RNA and miRNA host gene (miRNA HG) expression, influencing both their transcription and stability. Notably, SFPQ protects specific miRNA HGs, including the oncogenic miR-17~92 polycistron, from degradation by the nuclear NEXT-exosome complex. Lastly, we show that high SFPQ is tightly linked with overexpression miR-17~92 and its mature miRNAs across a broad variety of cancers. Our findings reveal a dual role for SFPQ in the regulation of miRNA HGs transcription and stability, as well as its significance in cancers.

2024-09-04 | GSE262127 | GEO

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