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BUD31 in ovarian cancer cells

ABSTRACT: BUD31 in ovarian cancer cells

PROVIDER: PRJNA760899 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15724215_1.fastq.gz	Fastqsanger.gz
	SRR15724215_2.fastq.gz	Fastqsanger.gz
	SRR15724216_1.fastq.gz	Fastqsanger.gz
	SRR15724216_2.fastq.gz	Fastqsanger.gz
	SRR15724217_1.fastq.gz	Fastqsanger.gz

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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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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 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.

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SpyCLIP sequencing of BUD31 in ovarian cancer cells

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

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