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RNAseq analysis of ESRP regulated splicing events in prostate cancer

ABSTRACT: RNAseq analysis of ESRP regulated splicing events in prostate cancer

PROVIDER: PRJNA531685 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8870780_1.fastq.gz	Fastqsanger.gz
	SRR8870780_2.fastq.gz	Fastqsanger.gz
	SRR8870781_1.fastq.gz	Fastqsanger.gz
	SRR8870781_2.fastq.gz	Fastqsanger.gz
	SRR8870782_1.fastq.gz	Fastqsanger.gz

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RNAseq analysis of ESRP regulated splicing events in prostate cancer

Project description:Progression of prostate cancer -the most frequent cancer in men- is driven by androgen steroid hormones, and delayed by androgen deprivation therapy (ADT). Androgens control transcription in prostate cancer cells by stimulating androgen receptor (AR) activity, but also control pre-mRNA splicing through less clear mechanisms. Here we examine whether androgens regulate splicing through AR-mediated transcriptional control of splicing regulator proteins. Supporting this mechanism we find AR controls ESRP2, which encodes a key epithelial-specific splicing regulator. Both ESRP2 and its close paralog ESRP1 are highly expressed in primary prostate cancer, and slow growth of prostate cancer xenografts in mice. Androgen stimulation induces splicing switches in many endogenous ESRP2-controlled mRNA isoforms, including a key splicing switch in the metastatic regulator FLNB which is associated with disease relapse after treatment. ESRP2 expression in clinical prostate cancer is repressed by ADT, which may thus inadvertently dampen epithelial splice programmes. Supporting this, FLNB splicing was reciprocally switched by the AR antagonist Casodex®. Our data reveal a new mechanism of splicing control in prostate cancer with important implications for disease progression.

2019-09-06 | GSE129540 | GEO

The epithelial splicing factors ESRP1 and ESRP2 positively and negatively regulate alternative splicing events

Project description:Epithelial Splicing Regulatory Proteins 1 and 2 (ESRP1 and ESRP2) are recently discovered epithelial-specific RNA-binding proteins that promote splicing of the epithelial variant of the FGFR2, ENAH, CD44, and CTNND1 transcripts. To catalogue a larger set of splicing events under the regulation of the ESRPs, we profiled splicing changes induced by RNA interference-mediated knockdown of ESRP1 and ESRP2 expression in a human epithelial cell line using the splicing-sensitive Affymetrix Exon ST1.0 Arrays. Analysis of the microarray data using the previously described MADS tool resulted in the identification of over a hundred candidate ESRP-regulated splicing events. We were able to independently validate 37 of these targets by RT-PCR. The ESRP-regulated events encompass all known types of alternative splicing events. Importantly, a number of these regulated splicing events occur in gene transcripts that encode proteins with well-described roles in the regulation of actin cytoskeleton organization, cell-cell adhesion, cell polarity, and cell migration. In sum, this work reveals a novel list of transcripts differentially spliced in epithelial and mesenchymal cells, implying that coordinated alternative splicing plays a critical role in determination of cell type identity. Keywords: control / knockdown comparison

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The epithelial splicing factors ESRP1 and ESRP2 positively and negatively regulate alternative splicing events

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An ESRP-regulated splicing program is abrogated during the Epithelial Mesenchymal Transition

Project description:Alternative splicing achieves coordinated changes in post-transcriptional gene expression programs through the activities of diverse RNA binding proteins. Epithelial Splicing Regulatory Proteins 1 and 2 (ESRP1 and ESRP2) are cell type-specific regulators of transcripts that switch splicing during the Epithelial Mesenchymal Transition (EMT). To define a comprehensive program of alternative splicing that is regulated during the EMT, we identified an extensive ESRP-regulated splicing network of hundreds of alternative splicing events within numerous genes with roles in cell-cell adhesion, polarity, and migration. Loss of this global ESRP-regulated epithelial splicing program induces the phenotypic changes in cell morphology that are observed during the EMT. Components of this splicing signature provide novel molecular markers that can be used to characterize the EMT. Bioinformatics and experimental approaches revealed a high affinity ESRP binding motif and a predictive RNA map that governs their activity. This work establishes the ESRPs as coordinators of a complex alternative splicing network that adds an important post-transcriptional layer to the changes in gene expression that underlie epithelial-mesenchymal transitions during development and disease. Keywords: control / knockdown comparison and control / ectopic expression comparison

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Project description:Tissue- and cell-type specific regulators of alternative splicing (AS) are an essential layer of posttranscriptional gene regulation necessary for normal cellular function, patterning, and development. Here we report the Epithelial splicing regulatory proteins (Esrps) are required for patterning of multiple organs, with loss of both paralogs, Esrp1 and Esrp2, resulting in increasingly severe phenotypes. Global profiling of the Esrp splicing regulatory network from total epidermis revealed varied splicing sensitivity of Esrp targets upon loss of Esrp1 or double knockout. This may explain the progressive phenotypes seen in Esrp knockout mice, and these mice provide a unique genetic tool to evaluate functional consequences of epithelial splicing events in vivo.

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