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SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α

ABSTRACT: SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α

PROVIDER: PRJNA831827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18910173_1.fastq.gz	Fastqsanger.gz
	SRR18910173_2.fastq.gz	Fastqsanger.gz
	SRR18910174_1.fastq.gz	Fastqsanger.gz
	SRR18910174_2.fastq.gz	Fastqsanger.gz
	SRR18913474.fastq.gz	Fastqsanger.gz

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Similar Datasets

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [RNA-Seq]

Project description:SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [RNA-Seq]

| PRJNA831709 | ENA

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [ChIP-Seq]

Project description:SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [ChIP-Seq]

| PRJNA831832 | ENA

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [RNA-Seq murine organoids]

Project description:SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [RNA-Seq murine organoids]

| PRJNA851799 | ENA

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [ChIP-Seq]

Project description:Splicing factor 3b subunit 1 (SF3B1) is one of the most frequently mutated spliceosomal components in cancer. Recent studies additionally imply an involvement of the wildtype protein in tumor progression, but the underlaying mechanism remains elusive. Here we report that SF3B1 acts as a coactivator for hypoxia-inducible factor (HIF) 1α. SF3B1 directly interacts with HIF1a, augments HIF1a-HIF1b heterodimer binding to hypoxia response elements in vivo and enhances transactivation of HIF target genes. In human patients, primary patient cells and in a mouse model of pancreatic ductal adenocarcinoma (PDAC), efficient HIF1a-signalling relies on SF3B1. Monoallelic deletion of Sf3b1 in this mouse tumor model severely delays tumor initiation and development and diminishes HIF target gene transcription, glucose uptake and proliferation in corresponding tumor organoids in hypoxia, while splicing remains functional. Here, we define a subset of aggressive chromophobe renal cell carcinomas (chRCCs) able to transcriptionally compensate monoallelic SF3B1 loss, a feature that correlates with poor prognosis and lymph node spread and we show that the oncogenic hotspot mutation SF3B1K700E has reduced co-activation efficiency. Also, we report increased sensitivity of cells with low levels of SF3B1 to the HIF-inhibitor PX-478. These findings reveal a splicing-independent, tumor promoting function of SF3B1, important in the pathogenesis of PDAC and other cancers.

2022-06-22 | GSE201461 | GEO

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [RNA-Seq]

2022-06-22 | GSE201427 | GEO

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α [RNA-Seq murine organoids]

2022-06-25 | GSE206703 | GEO

SF3B1 promotes glycolysis and tumor malignancy through splicing-independent activation of HIF1α

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

2022-06-22 | GSE201462 | GEO

SF3B1 Degron knockdown RNA-seq

Project description:Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.

2015-03-11 | E-GEOD-66719 | biostudies-arrayexpress

SF3B1

Project description:SF3B1

| PRJNA848802 | ENA

SF3B1 association with chromatin determines splicing outcomes

Project description:Much remains unknown concerning the mechanism by which the splicing machinery pinpoints short exons within intronic sequences and how splicing factors are directed to their pre-mRNA targets. Part of the explanation probably lies in differences in chromatin organization between exons and introns. Proteomic, co-immunoprecipitation, and sedimentation analyses described here indicated that SF3B1, an essential splicing component of the U2 snRNP complex, is strongly associated with nucleosomes. ChIP-seq and RNA-seq analyses revealed that SF3B1 is specifically bound to nucleosomes located at exonic positions. SF3B1 binding is enriched at nucleosomes positioned over short exons flanked by long introns that are also characterized by differential GC content between exons and introns. Disruption of SF3B1 binding to such nucleosomes affected the splicing of these exons similarly to inhibition of SF3B1 expression. Our findings suggest that the association of SF3B1 with nucleosomes is functionally important for splice site recognition and that SF3B1 conveys splicing-relevant information embedded in chromatin structure. MNase-seq on Input and SF3B1 pull-down, mRNA-seq on control and SF3B1 si-RNA treated cells as well as on TSA (Trichostatin A) treated and untreated cells.

2015-04-22 | E-GEOD-65644 | biostudies-arrayexpress

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