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DSCAM-AS1-driven proliferation of breast cancer cells involves regulation of alternative exon splicing and 3’-end usage

ABSTRACT: DSCAM-AS1-driven proliferation of breast cancer cells involves regulation of alternative exon splicing and 3’-end usage

PROVIDER: PRJNA632880 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11790860_1.fastq.gz	Fastqsanger.gz
	SRR11790860_2.fastq.gz	Fastqsanger.gz
	SRR11790861_1.fastq.gz	Fastqsanger.gz
	SRR11790861_2.fastq.gz	Fastqsanger.gz
	SRR11790862_1.fastq.gz	Fastqsanger.gz

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DSCAM-AS1-driven proliferation of breast cancer cells involves regulation of alternative exon splicing and 3’-end usage

Project description:Background: DSCAM-AS1 is a cancer-related long noncoding RNA with higher expression levels in Luminal A, B and HER2-positive Breast Cancer (BC), where its expression is strongly dependent on Estrogen Receptor Alpha (ERα). Method: To decipher its function, DSCAM-AS1 expression was measured by qRT-PCR in tissue samples from 93 BC patients in addition to a meta-analysis of 30 gene expression datasets, together with the evaluation of its association with clinical data. By computational analyses of our RNA-Seq in MCF-7 cells, we investigated the DSCAM-AS1 knock-down effects at both gene and isoform levels Results: We confirmed DSCAM-AS1 overexpression in high grade Luminal A, B and HER2+ BCs and found a significant correlation with disease relapse. 908 genes were regulated by DSCAM-AS1-silencing, primarily involved in cell cycle and inflammatory response. Noteworthy, the analysis of alternative splicing and isoform regulation revealed 2,085 splicing events regulated by DSCAM-AS1, enriched in differential polyadenylation sites and 3’UTR shortening events. Finally, the DSCAM-AS1-interacting splicing factor hnRNPL was predicted as the most enriched RBP for exon skipping and 3’UTR events. Conclusion: The relevance of DSCAM-AS1 overexpression in BC is confirmed by clinical data and further enhanced by its possible involvement in the regulation of RNA processing, which is emerging as one of the most important dysfunctions in cancer.

2020-05-15 | GSE150591 | GEO

Neuronal activity regulates alternative exon usage

Project description:Neuronal activity regulates alternative exon usage

| PRJNA622919 | ENA

DSCAM-AS1-Driven Proliferation of Breast Cancer Cells Involves Regulation of Alternative Exon Splicing and 3'-End Usage.

Project description:DSCAM-AS1 is a cancer-related long noncoding RNA with higher expression levels in Luminal A, B, and HER2-positive Breast Carcinoma (BC), where its expression is strongly dependent on Estrogen Receptor Alpha (ERα). DSCAM-AS1 expression is analyzed in 30 public datasets and, additionally, by qRT-PCR in tumors from 93 BC patients, to uncover correlations with clinical data. Moreover, the effect of DSCAM-AS1 knockdown on gene expression and alternative splicing is studied by RNA-Seq in MCF-7 cells. We confirm DSCAM-AS1 overexpression in high grade Luminal A, B, and HER2+ BCs and find a significant correlation with disease relapse. In total, 908 genes are regulated by DSCAM-AS1-silencing, primarily involved in the cell cycle and inflammatory response. Noteworthily, the analysis of alternative splicing and isoform regulation reveals 2085 splicing events regulated by DSCAM-AS1, enriched in alternative polyadenylation sites, 3'UTR (untranslated region) shortening and exon skipping events. Finally, the DSCAM-AS1-interacting splicing factor heterogeneous nuclear ribonucleoprotein L (hnRNPL) is predicted as the most enriched RBP for exon skipping and 3'UTR events. The relevance of DSCAM-AS1 overexpression in BC is confirmed by clinical data and further enhanced by its possible involvement in the regulation of RNA processing, which is emerging as one of the most important dysfunctions in cancer.

| S-EPMC7352480 | biostudies-literature

KIS counteracts PTBP2 and regulates alternative exon usage in neurons

Project description:Alternative RNA splicing is an essential and dynamic process in neuronal differentiation and synapse maturation, and dysregulation of this process has been associated with neurodegenerative diseases. Recent studies have revealed the importance of RNA-binding proteins in the regulation of neuronal splicing programs. However, the molecular mechanisms involved in the control of these splicing regulators are still unclear. Here we show that KIS, a kinase upregulated in the developmental brain, imposes a genome-wide alteration in exon usage during neuronal differentiation. KIS contains a protein-recognition domain common to spliceosomal components and phosphorylates PTBP2, counteracting the role of this splicing factor in exon exclusion. At the molecular level, phosphorylation of unstructured domains within PTBP2 causes its dissociation from two co-regulators, Matrin3 and hnRNPM, and hinders the RNA-binding capability of the complex. Furthermore, KIS and PTBP2 display strong and opposing functional interactions in synaptic spine emergence and maturation. Taken together, our data uncover a post-translational control of splicing regulators that link transcriptional and alternative exon usage programs in neuronal development.

2024-04-25 | PXD050320 | Pride

Global Promotion of Alternative Internal Exon Usage by mRNA 3' End Formation Factors

Project description:Global Promotion of Alternative Internal Exon Usage by mRNA 3' End Formation Factors

| PRJNA258164 | ENA

KIS counteracts PTBP2 and regulates alternative exon usage in neurons

Project description:KIS counteracts PTBP2 and regulates alternative exon usage in neurons

| PRJNA1083502 | ENA

Luminal lncRNAs Regulation by ERα-controlled Enhancers in a Ligand-independent Manner in Breast Cancer Cells

Project description:Estrogen receptor-α (ERα) is a ligand-inducible protein which mediates estrogenic hormones signaling and defines the luminal breast cancer phenotype. Recently, we demonstrated that ERα binds chromatin in absence of ligand (apoERα) regulating transcription of protein-coding genes and several lncRNAs. Noteworthy, apoERα-regulated lncRNAs marginally overlap estrogen-induced transcripts representing a signature of luminal breast cancer genes. DSCAM-AS1 is a paradigmatic example of apoERα activity since its expression is largely unaffected by estrogenic treatment despite an E2-induced increment of ERα binding on its promoter. Analysing H3K27ac ChIP-Seq performed in hormone-deprived MCF-7, we identified a set of Super Enhancers (SEs) occupied by apoERα including one mapped in proximity of DSCAM-AS1. Using ChIP-qPCR, we validated ChIP-Seq signal of apoERα, p300 and CTCF at both DSCAM-AS1 TSS and at its associated SE. Furthermore, analysing MCF-7 ChIA-PET data and performing a 3C experiment, we confirmed a long range chromatin interaction between the SE and the DSCAM-AS1 TSS. Interestingly, CTCF binding downstream to DSCAM-AS1 shows an enrichment in hormone-depleted medium as compared to other experimental conditions, indicating that CTCF demarcates enhancer actions at DSCAM-AS1 locus. The analysis of this lncRNA provides a paradigm of transcriptional regulation of a luminal specific apoERα regulated lncRNA.

2018-02-06 | GSE108693 | GEO

ArgRS, MetRS, and SRRM2 dependent changes in mRNA splicing and exon usage

Project description:ArgRS, MetRS, and SRRM2 dependent changes in mRNA splicing and exon usage

| PRJNA694846 | ENA

Inflammation drives alternative first exon usage of critical immune genes including Aim2

Project description:Inflammation drives alternative first exon usage of critical immune genes including Aim2

| PRJNA594622 | ENA

Effects of SOCS2-AS1 inhibition in prostate cancer cells

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. We identified a novel androgen-regulated long non-coding (lnc) RNA, SOCS2-AS1. In order to investigate the SOCS2-AS1 function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines (LNCaP and LTAD) after siSOCS2-AS1 or siSOCS2 treatment. We also treated cells with vehicle or androgen to analyzed the effects of siSOCS2-AS1 on AR function. Observation of androgen dependent gene expression changes after treatmet with siSOCS2-AS1 with microarray.

2016-08-01 | E-GEOD-82224 | biostudies-arrayexpress

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