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Identification of FUBP1 as a long tail driver and widespread regulator of tumor suppressor and oncogene alternative splicing

ABSTRACT: Identification of FUBP1 as a long tail driver and widespread regulator of tumor suppressor and oncogene alternative splicing

PROVIDER: PRJNA505136 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8180980_1.fastq.gz	Fastqsanger.gz
	SRR8180980_2.fastq.gz	Fastqsanger.gz
	SRR8180981_1.fastq.gz	Fastqsanger.gz
	SRR8180981_2.fastq.gz	Fastqsanger.gz
	SRR8180982_1.fastq.gz	Fastqsanger.gz

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Identification of FUBP1 as a long tail driver and widespread regulator of tumor suppressor and oncogene alternative splicing

Project description:Comprehensive sequencing approaches have allowed for the identification of the most frequent contributors to cancer, known as drivers. They have also revealed a class of mutations in understudied, infrequently altered genes, referred to as “long tail” (LT) drivers. A key challenge has been to find clinically relevant LT drivers and understand how they cooperate to drive disease. Here, we identified Far Upstream Binding Protein 1 (FUBP1) as a LT driver using an in vivo CRISPR screen. FUBP1 cooperates with other tumor suppressor genes to transform mammary epithelial cells by disrupting cellular differentiation and tissue architecture. Mechanistically, FUBP1 participates in regulating m6A RNA methylation, and its loss leads to global changes in RNA splicing and widespread expression of aberrant driver isoforms. These findings suggest that somatic alteration of a single gene involved in RNA splicing and m6A methylation can produce the necessary panoply of contributors for neoplastic transformation.

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Identification of FUBP1 as a Long Tail Cancer Driver and Widespread Regulator of Tumor Suppressor and Oncogene Alternative Splicing.

Project description:Comprehensive sequencing approaches have allowed for the identification of the most frequent contributors to cancer, known as drivers. They have also revealed a class of mutations in understudied, infrequently altered genes, referred to as "long tail" (LT) drivers. A key challenge has been to find clinically relevant LT drivers and to understand how they cooperate to drive disease. Here, we identified far upstream binding protein 1 (FUBP1) as an LT driver using an in vivo CRISPR screen. FUBP1 cooperates with other tumor suppressor genes to transform mammary epithelial cells by disrupting cellular differentiation and tissue architecture. Mechanistically, FUBP1 participates in regulating N6-methyladenosine (m6A) RNA methylation, and its loss leads to global changes in RNA splicing and widespread expression of aberrant driver isoforms. These findings suggest that somatic alteration of a single gene involved in RNA splicing and m6A methylation can produce the necessary panoply of contributors for neoplastic transformation.

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Fubp1 knockdown in BCR-ABL1 induced chronic myeloid leukemia (CML) like myeloproliferative neoplasm mouse model

Project description:We examine the oncogenic function of the Far Upstream Element Binding Protein 1 (FUBP1) in leukemia-initiating cells. For this perpose we performed knockdown of Fubp1 in CML cells in our mouse model. Here, we transduce donor bone marrow cell with the oncogene BCR-ABL1 and Fubp1 or scrambled shRNA and transplanted in recipient mice. Lineage- BCR-ABL1+ shRNA+ cells were then sorted from diseased mice and analyzed by RNA sequencing. We compare the gene expression of the Fubp1 shRNA expressing CML cells versus the control (scrambled shRNA expressing) cells in order to identify the relevant Fubp1 target genes.

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FUBP1 is a core splicing factor that facilitates 3' splice site recognition and splicing of long introns [RNA-Seq]

Project description:Splicing is a central process in metazoans and greatly expands their proteome by alternative splicing of pre-mRNA transcripts. An essential regulatory step during early spliceosome assembly is the recognition of cis-regulatory RNA motifs in pre-mRNAs. Here, we identified the RNA binding protein FUBP1 as a novel core splicing factor with a ubiquitous footprint on pre-mRNAs. FUBP1 binds to a previously unknown cis-regulatory motif upstream of the branch point of human introns. We show that FUBP1 binds and stabilises known 3' splice site components such as the essential splicing factor U2AF2. FUBP1 mutant cell lines and patient data indicate that FUBP1 is particularly relevant for efficient splicing of exons flanked by long introns. In addition to its role at the 3’ splice site, FUBP1 shows multiple interactions with U1 snRNP- associated proteins. This demonstrates an important role for FUBP1 in splice site bridging in the context of long introns.

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FUBP1 is a core splicing factor that facilitates 3' splice site recognition and splicing of long introns [In vivo iCLIP]

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FUBP1 is a core splicing factor that facilitates 3' splice site recognition and splicing of long introns [In vitro iCLIP]

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FUBP1 and FUBP2 enforce distinct epigenetic setpoints for MYC expression in primary single murine cells

Project description:We used ChIP-seq to assess where FUBP1 binds to MYC gene in the mouse genome

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Project description:Transcriptomic profiling classifies pancreatic ductal adenocarcinoma (PDAC) into several molecular subtypes with distinctive histological and clinical characteristics. However, little is known about the molecular mechanisms that define each subtype and how this correlates with clinical outcome. Mutant KRAS is the most prominent driver in PDAC, present in over 90% of tumors, but the dependence of tumors on oncogenic KRAS signaling varies between subtypes. In particular, squamous subtype PDACs are relatively independent of oncogenic KRAS signaling and typically display much more aggressive clinical behavior versus progenitor subtype PDACs. Here, we identified that YAP1 activation is enriched in the squamous subtype and associated with poor prognosis. Activation of YAP1 in progenitor subtype cancer cells profoundly enhanced malignant phenotypes and transformed progenitor subtype cells into squamous subtype. Conversely, depletion of YAP1 specifically suppressed tumorigenicity of squamous subtype PDAC tumors. Mechanistically, we uncovered a significant positive correlation between WNT5A expression and the YAP activation signature, and we demonstrated that WNT5A overexpression led to YAP activation and recapitulated YAP1-dependent but but Kras-independent phenotype of tumor progression and maintenance. Thus, our study identifies YAP1 oncogene as a major driver of squamous subtype PDAC and uncovers the role of WNT5A to drive PDAC malignancy via activation of the YAP pathway.

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