RNA sequencing (RNA-seq) of BUD31 knockdown or overexpression in ovarian cancer cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA760902 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15724257_1.fastq.gz | Fastqsanger.gz | |||
| SRR15724257_2.fastq.gz | Fastqsanger.gz | |||
| SRR15724258_1.fastq.gz | Fastqsanger.gz | |||
| SRR15724258_2.fastq.gz | Fastqsanger.gz | |||
| SRR15724259_1.fastq.gz | Fastqsanger.gz |
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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.
2022-09-19 | GSE183449 | GEO
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
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.
2022-09-19 | GSE183451 | GEO
Project description:RNA immunoprecipitation sequencing (RIP-seq) of BUD31 in ovarian cancer cells
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Project description:SpyCLIP sequencing of BUD31 in ovarian cancer cells
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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.
2022-11-04 | GSE189715 | GEO
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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Project description:The high frequency of somatic copy number alterations, as opposed to point mutations, is considered a unique feature of high-grade serous ovarian carcinoma (HGSOC). Amplification-dependent overexpression of RECQL4, which participates in DNA replication and repair, mediates the development of various cancers, but its pathobiological and clinical roles are poorly understood. Here, using bioinformatics analysis, RECQL4 amplification was found to occur in 27% of HGSOC samples in the TCGA cohort. RECQL4 was found to be upregulated and associated with a poor prognosis based on the immunohistochemistry staining of HGSOC. Functionally, RECQL4 overexpression increased proliferation and invasion of ovarian cancer cells both in vitro and in vivo. RECQL4 silencing had the opposite effects. In addition, RECQL4 knockdown enhanced the sensitivity of ovarian cancer cells to cisplatin and PARP inhibitor (PARPi). Further mechanistic investigations revealed that MAFB was a downstream target of RECQL4. The oncogenic effect of RECQL4 was attenuated after MAFB knockdown. Moreover, RECQL4 overexpression was negatively regulated by the tumour suppressor miR-10a-5p. Collectively, these findings indicate that genomic amplification and low expression of miR-10a-5p contribute to RECQL4 overexpression in ovarian cancer. This is the first study to reveal the oncogenic functions and clinical significance of RECQL4 in ovarian cancer.
2020-10-13 | GSE153839 | GEO
Project description:Proteomes of Mycoplasma gallisepticum strains with overexpression and knockdown of WhiA transcription factor. The overexpression was introduced on a transposon vector carrying M. gallisepticum whiA gene with strong constitutive promoter and strong SD sequence. The knockdown was made by CRISPRi. dCas9 protein and sgRNA against whiA gene were introduced on a transposon vector.
2021-06-25 | PXD026928 | Pride