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Consequences of SF3B1 mutation on the proteome

ABSTRACT: In this study, we evaluated the differential proteome of SF3B1-mutated and SF3B1-Wild-Type uveal melanoma cells (isogenic Mel202 cells). We performed a quantitative label-free tandem liquid chromatography mass spectrometry (LC-MS/MS) analysis of SF3B1WT and SF3B1mut Mel202 cells.

INSTRUMENT(S): Q Exactive HF-X

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Uveal Melanoma Cell

SUBMITTER: Valentin SABATET

LAB HEAD: Damarys Loew

PROVIDER: PXD022726 | Pride | 2022-03-15

REPOSITORIES: Pride

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			Action	DRS
	Design.xls	Xls
	H0540BL.msf	Msf
	H0540BL.raw	Raw
	H0541BL.msf	Msf
	H0541BL.raw	Raw

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Transcriptomic analyses of primary uveal melanomas

Project description:SF3B1 is coding an essential splicing factor. This gene was found recurrently mutated in uveal melanoma. To understand the consequences of these hotspot SF3B1 mutations, we performed high coverage RNA-seq on 74 primary uveal melanomas, which were treated by primary enucleation. We analyzed data for aberrant splicing in relation with SF3B1 status.

2016-07-03 | E-MTAB-4097 | biostudies-arrayexpress

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 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.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scRNA-seq]

Project description:Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scADT-seq]

Project description:Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scTCR-seq]

Project description:Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [bulk TCR-seq]

Project description:Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

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Transcriptome analysis of chronic lymphoid leukemia reveals isoform regulation associated with mutations in SF3B1

Project description:Several DNA sequencing studies of chronic lymphocytic leukemia (CLL) revealed that the splicing factor SF3B1 accumulated somatic point mutations in about 10 percent of the patients. In most cases the mutations were located in the genomic regions coding for the C-terminal HEAT-repeat domain and in many cases, the mutations gave rise to specific amino acid substitutions. Here, we aimed to investigate differential usage of exons associated with the mutation K700E of SF3B1 in CLL tumuor cells. We generated RNA-Seq transcriptome data from two patients with mutations in SF3B1, two patient without mutations in SF3B1 and from healthy donors. We report interesting examples and possible consequences of the alternative exon usage in these genes. This dataset contains only the files resulting from the processing the RNA sequencing raw data. This avoids potential patient identifiability, but ensures the full reproducibility of the results described in the publication.

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2016-01-15 | E-GEOD-67736 | biostudies-arrayexpress

Mutant SF3B1 promotes AKT and NF-kB driven mammary tumorigenesis

Project description:Mutations in the core RNA splicing factor SF3B1 are prevalent in leukemias and uveal melanoma, but also recurrent in epithelial malignancies such as breast cancer. Whereas hotspot mutations in SF3B1 alter hematopoietic differentiation, whether SF3B1 mutations contribute to epithelial cancer development and progression is unknown. Here, we identify that SF3B1 mutations in mammary epithelial and breast cancer cells induce a recurrent pattern of aberrant splicing leading to activation of AKT and NF-kB, enhanced cell migration, and accelerated tumorigenesis. Transcriptomic analysis of human cancer specimens, MMTV-cre Sf3b1K700E/WT mice, and isogenic mutant cell lines identified hundreds of aberrant 3’ splice sites induced by mutant SF3B1, a portion of which were breast-specific. Across mouse and human tumors, mutant SF3B1 promoted aberrant splicing (dependent on aberrant branchpoints as well as pyrimidines downstream of the aberrant branchpoint) and consequent suppression of PPP2R5A and MAP3K7, critical negative regulators of AKT and NF-kB. Coordinate activation of NF-kB and AKT signaling was observed in the knock-in models, leading to accelerated cell migration and tumor development in combination with mutant PIK3CA but also hypersensitizing cells to AKT kinase inhibitors. These data identify mutations in SF3B1 as drivers of breast tumorigenesis and reveal unique vulnerabilities in cancers harboring them.

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