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Death Associated Protein 3 (DAP3) Coordinates Splicing Regulatory Networks to Modulate Global Alternative Splicing in Cancer

ABSTRACT: Death Associated Protein 3 (DAP3) Coordinates Splicing Regulatory Networks to Modulate Global Alternative Splicing in Cancer

PROVIDER: PRJNA721961 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14238937_1.fastq.gz	Fastqsanger.gz
	SRR14238937_2.fastq.gz	Fastqsanger.gz
	SRR14238938_1.fastq.gz	Fastqsanger.gz
	SRR14238938_2.fastq.gz	Fastqsanger.gz
	SRR14238939_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Death Associated Protein 3 (DAP3) Coordinates Splicing Regulatory Networks to Modulate Global Alternative Splicing in Cancer

Project description:The dynamic regulation of transcriptome requires coordinated participation of multiple RNA binding proteins (RBPs) in RNA processing. Dysregulated RNA processing, such as aberrant alternative splicing, is implicated in many cancers. Therefore, it is critical to explore the cancer-related RNA processing regulation and the underlying mechanisms. Many RBPs lack classical RNA-binding domains and their functions in RNA processing regulation remain unclear. Through an unbiased transcriptome-wide analysis, we report DAP3 binds ubiquitously to endogenous RNAs in vivo and its depletion reshapes the alternative splicing landscape in cancer cells. Mechanistically, we show DAP3 coordinates splicing regulatory networks, not only via mediating the formation of ribonucleoprotein (RNP) complexes, but also via modulating splicing of numerous splicing factors. Specific DAP3-regulated splicing changes such as non-productive splicing of WSB1 and RBM6, play important roles in tumorigenesis. Together, these findings provide critical mechanistic insights into the molecular functions of DAP3 in cancer development as a master regulator of RNA processing.

2022-02-10 | GSE172078 | GEO

Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

Project description:RNA editing introduces nucleotide changes in RNA sequences. Recent studies have reported that aberrant A-to-I RNA editing profiles are implicated in cancers. Albeit changes in expression and activity of ADAR genes are thought to have been responsible for the dysregulated RNA editome in diseases, they are not always correlated, indicating the involvement of secondary regulators. Here, we uncover DAP3 as a potent repressor of editing and a strong oncogene in cancer. DAP3 mainly interacts with the deaminase domain of ADAR2 and represses editing via disrupting association of ADAR2 with its target transcripts. PDZD7, an exemplary DAP3-repressed editing target, undergoes a protein recoding editing at stop codon [Stop →Trp (W)]. Because of editing suppression by DAP3, the unedited PDZD7WT, which is more tumorigenic than edited PDZD7Stop518W, is accumulated in tumors. In sum, cancer cells may acquire malignant properties for their survival advantage through suppressing RNA editome by DAP3.

2020-06-23 | GSE123020 | GEO

Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3)

Project description:Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3)

| PRJNA994439 | ENA

Discovery of DAP3-binding RNA sites by eCLIP

Project description:eCLIP paired-end sequencing of DAP3 in EC109 cells with two biological replicates. This analysis revealed the genome-wide RNA binding landscape of DAP3, as the supporting data of the main publication.

2020-06-23 | GSE144318 | GEO

Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3) [eCLIP-seq]

Project description:Modulation of m6A RNA Methylation by Death Associated Protein 3 (DAP3) [eCLIP-seq]

| PRJNA994837 | ENA

Bacteria modulate tamoxifen-induced death via host fatty acid metabolism

Project description:Bacteria modulate tamoxifen-induced death via host fatty acid metabolism

| PRJNA776017 | ENA

Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

Project description:Suppression of adenosine-to-inosine (A-to-I) RNA editome by death associated protein 3 (DAP3) promotes cancer progression

| PRJNA507260 | ENA

Bacteria modulate tamoxifen-induced death via host fatty acid metabolism

Project description:Our microbiota affects numerous processes involved in development, health, and the response to chemotherapeutic drugs. Tamoxifen is a selective estrogen receptor (ER) modulator that is used to treat ER positive breast cancer, but that at high doses kills both ER positive and ER-negative breast cancer cells. We recapitulate this off-target effect in Caenorhabditis elegans, which does not have an ER ortholog. We find that different bacteria dramatically modulate tamoxifen toxicity in C. elegans, with a three-order of magnitude difference between animals fed Escherichia coli, Comamonas aquatica, and Bacillus subtilis. Remarkably, host fatty acid (FA) biosynthesis mitigates tamoxifen toxicity, and different bacteria provide the animal with different FAs, resulting in distinct FA profiles. Surprisingly these bacteria modulate tamoxifen toxicity by different death mechanisms, some of which are modulated by FA supplementation and others by antioxidants. Together, this work reveals a complex interplay between bacteria, FA metabolism and tamoxifen toxicity that may provide a blueprint for similar studies in more complex mammals.

2022-08-23 | GSE186785 | GEO

Discovery of DAP3-binding RNA sites by eCLIP

Project description:Discovery of DAP3-binding RNA sites by eCLIP

| PRJNA603360 | ENA

Food-derived Compounds Apigenin and Luteolin Modulate mRNA Splicing of Introns with Weak Splice Sites

Project description:Cancer cells often exhibit extreme sensitivity to splicing inhibitors. We identified food-derived flavonoids, apigenin and luteolin, as compounds that modulate mRNA splicing at the genome-wide level, followed by proliferation inhibition. They bind to mRNA splicing-related proteins to induce a widespread change of splicing patterns in treated cells. Their inhibitory activity on splicing is relatively moderate, and introns with weak splice sites tend to be sensitive to them. Such introns remain unspliced, and the resulting intron-containing mRNAs are retained in the nucleus, resulting in the nuclear accumulation of poly(A)+ RNAs in these flavonoid-treated cells. Tumorigenic cells are more susceptible to these flavonoids than non-tumorigenic cells, both for the nuclear poly(A)+ RNA-accumulating phenotype and cell viability. This study illustrates the possible mechanism of these flavonoids to suppress tumor progression in vivo that were demonstrated by previous studies, and provides the potential of daily intake of moderate splicing inhibitors to prevent cancer development.

2019-11-25 | GSE128097 | GEO

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