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Publication

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

Cell reports | 2019

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.

Pubmed ID: 31553912 RIS Download

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Associated grants

Agency: NIGMS NIH HHS, United States
Id: R01 GM124491
Agency: Howard Hughes Medical Institute, United States
Agency: NIGMS NIH HHS, United States
Id: T32 GM007753
Agency: NCI NIH HHS, United States
Id: R01 CA170851
Agency: NICHD NIH HHS, United States
Id: R01 HD073035
Agency: Cancer Research UK, United Kingdom

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This is a list of tools and resources that we have found mentioned in this publication.

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