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RNA immunoprecipitation sequencing (RIP-seq) of BUD31 in ovarian cancer cells

ABSTRACT: RNA immunoprecipitation sequencing (RIP-seq) of BUD31 in ovarian cancer cells

PROVIDER: PRJNA760901 | ENA |

REPOSITORIES: ENA

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RNA immunoprecipitation sequencing (RIP-seq) 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. RNA immunoprecipitation sequencing (RIP-seq) was used to analysis the interaction between BUD31 and the target RNA. Our data indicate that BUD31 is a critical oncogenic splicing factor in ovarian cancer and might act as a potential therapeutic target.

2022-09-19 | GSE183450 | GEO

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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RNA Immunoprecipitation(RIP)-seq of BUD31 in the mouse reproductive system

Project description:The testis is the organ with the most transcriptome diversity and alternative splicing (AS) is considered to be the most important source. However, the physiological role of AS in spermatogenesis is poorly understood. Here, we report that spliceosome component BUD31 is a prominent AS regulator in early stage of spermatogenesis in mice. Bud31 expression in the testis is initiated soon after birth. Conditional knock out of Bud31 in germ cells in Vasa-Cre mice led to loss of spermatogonial stem cells (SSCs) and to infertility. We further demonstrate that BUD31was required for both SSC pool maintenance and initiation of spermatogenesis. Mechanistically, BUD31 regulates the alternative splicing of multiple genes involved in cell cycle checkpoint and cell differentiation. In particular, we identified CDK2 as a direct splicing target of BUD31 through integrative analysis of SMART-seq and RIP-seq data. Knockout of BUD31 results in the intron retention as well as exon skipping of CDK2, which led to decrease in CDK2 expression. Our findings highlight the significance of BUD31 and its regulated AS in SSC self-renewal and differentiation.

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RNA sequencing (RNA-seq) of BUD31 knockdown or overexpression 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. 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.

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RNA Immunoprecipitation(RIP)-seq of BUD31 in the mouse reproductive system

Project description:RNA Immunoprecipitation(RIP)-seq of BUD31 in the mouse reproductive system

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