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RNA sequencing (RNA-seq) of BUD31 knockdown or overexpression in ovarian cancer cells

ABSTRACT: Mis-regulation of splicing factors are thought to activate cancer specific splicing programs that contribute to cancer development and progression. However, it remains a major challenge to identify the key splicing variants caused by aberrant expression of splicing factors in cancer. Here we report that splicing factor BUD31 is commonly overexpressed in high-grade serous ovarian carcinoma (HGSOC) and high level of BUD31 is associated with poor prognosis. RNA-seq analysis reveals that BUD31 inhibition predominantly results in alternation of exon skipping and intron retention. We further identify binding motif and preferred genome-wide binding pattern of BUD31 by CLIP-seq analysis. In particular, we demonstrate that BUD31 overexpression drives an oncogenic splicing switch of BCL2L12 (an anti-apoptotic BCL2 family member) to produce a full-length isoform (BCL2L12-L) which in turn increased the survival, proliferation and anti-apoptosis ability of ovarian cancer cells. Our data indicate that BUD31 is a critical oncogenic splicing factor in ovarian cancer and might act as a potential therapeutic target.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183449 | GEO | 2022/09/19

REPOSITORIES: GEO

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SpyCLIP sequencing of BUD31 in ovarian cancer cells

Project description:Mis-regulation of splicing factors are thought to activate cancer specific splicing programs that contribute to cancer development and progression. However, it remains a major challenge to identify the key splicing variants caused by aberrant expression of splicing factors in cancer. Here we report that splicing factor BUD31 is commonly overexpressed in high-grade serous ovarian carcinoma (HGSOC) and high level of BUD31 is associated with poor prognosis. RNA-seq analysis reveals that BUD31 inhibition predominantly results in alternation of exon skipping and intron retention. We further identify binding motif and preferred genome-wide binding pattern of BUD31 by CLIP-seq analysis. Our data indicate that BUD31 is a critical oncogenic splicing factor in ovarian cancer and might act as a potential therapeutic target.

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BUD31 in ovarian cancer cells

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Oncogenic MYC induces a dependency on the spliceosome in human cancer

Project description:c-MYC (MYC) overexpression or hyperactivation is one of the most common drivers of human cancer. Despite intensive study, the MYC oncogene remains recalcitrant to therapeutic inhibition. Like other classic oncogenes, hyperactivation of MYC leads to collateral stresses onto cancer cells, suggesting that tumors harbor unique vulnerabilities arising from oncogenic activation of MYC. Herein, we discover the spliceosome as a new target of oncogenic stress in MYC-driven cancers. We identify BUD31 as a MYC-synthetic lethal gene, and demonstrate that BUD31 is a splicing factor required for the assembly and catalytic activity of the spliceosome. Core spliceosomal factors (SF3B1, U2AF1, and others) associate with BUD31 and are also required to tolerate oncogenic MYC. Notably, MYC hyperactivation induces an increase in total pre-mRNA synthesis, suggesting an increased burden on the core spliceosome to process pre-mRNA. In contrast to normal cells, partial inhibition of the spliceosome in MYC-hyperactivated cells leads to global intron retention, widespread defects in pre-mRNA maturation, and deregulation of many essential cell processes. Importantly, genetic or pharmacologic inhibition of the spliceosome in vivo impairs survival, tumorigenicity, and metastatic proclivity of MYC-dependent breast cancers. Collectively, these data suggest that oncogenic MYC confers a collateral stress on splicing and that components of the spliceosome may be therapeutic entry points for aggressive MYC-driven cancers. Examination of intron rentention in MYC-ER HMECs, in 4 conditions

2015-09-03 | E-GEOD-66182 | biostudies-arrayexpress

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