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The effect of REST and its alternatively spliced transcript, REST-003, on breast cancer invasiveness

ABSTRACT: The effect of REST and its alternatively spliced transcript, REST-003, on breast cancer invasiveness

PROVIDER: PRJNA268443 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1662260.fastq.gz	Fastqsanger.gz
	SRR1662261.fastq.gz	Fastqsanger.gz
	SRR1662262.fastq.gz	Fastqsanger.gz
	SRR1662263.fastq.gz	Fastqsanger.gz
	SRR1662254.fastq.gz	Fastqsanger.gz

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Effect of REST on cancer invasiveness in MCF-7 and MDA-MB-231 cells using RNA-sequencing (RNA-seq) analysis .

Project description:We report a negative correlation of invasiveness with REST expression. In addition, one alternatively spliced product (ASP) of REST, REST-003, shows a positive correlation with invasiveness. REST has a well-established role in regulating transcription of genes important for neuronal development. Its role in cancer, though significant, is less well understood. We would like to investigate the effect of REST on invasive phenotype. In order to do so, we downregulate REST by siRNA treatment in weakly invasive MCF-7 breast cancer cells in which REST is expressed highly: 1) si-GAPDH (control), two si-RESTs (2)si-REST_1 and 3) si-REST_2). Conversely, we overexpress REST by transfection of wt-REST cDNA in highly invasive MDA-MB-231 cells in which REST is expressed at the low level: 4) EGFP (control), 5) mt-REST (another control) and 6) wt-REST. REST (repressor element-1 (RE-1) silencing transcription factor) contains a DNA-binding domain that is localized within eight zinc fingers and two repressor domains located at the N-terminal and C-terminal, respectively. REST suppresses expression of neural-specific genes. mt-REST lacks two repressor domains, so it can be used as a control for wt-REST. In contrast, REST-003 is one of alternatively spliced products (ASPs) of REST.

2014-12-01 | GSE63608 | GEO

Non-coding RNAs derived from an alternatively spliced REST transcript (REST-003) regulate breast cancer invasiveness.

Project description:RE1-Silencing Transcription factor (REST) has a well-established role in regulating transcription of genes important for neuronal development. Its role in cancer, though significant, is less well understood. We show that REST downregulation in weakly invasive MCF-7 breast cancer cells converts them to a more invasive phenotype, while REST overexpression in highly invasive MDA-MB-231 cells suppresses invasiveness. Surprisingly, the mechanism responsible for these phenotypic changes does not depend directly on the transcriptional function of REST protein. Instead, it is driven by previously unstudied mid-size (30-200 nt) non-coding RNAs (ncRNAs) derived from the first exon of an alternatively spliced REST transcript: REST-003. We show that processing of REST-003 into ncRNAs is controlled by an uncharacterized serine/arginine repeat-related protein, SRRM3. SRRM3 expression may be under REST-mediated transcriptional control, as it increases following REST downregulation. The SRRM3-dependent regulation of REST-003 processing into ncRNAs has many similarities to recently described promoter-associated small RNA-like processes. Targeting ncRNAs that control invasiveness could lead to new therapeutic approaches to limit breast cancer metastasis.

| S-EPMC4459148 | biostudies-literature

The effect of REST and its alternatively spliced transcript, REST-003, on breast cancer invasiveness

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-12-01 | GSE63610 | GEO

Glycine max Alternatively Spliced Transcript Detecting Microarray (GmASDM).

Project description:Glycine max Alternatively Spliced Transcript Detecting Microarray (GmASDM).

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An alternatively spliced p62 isoform promotes breast cancer chemoresistance

Project description:An alternatively spliced p62 isoform promotes breast cancer chemoresistance

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Mutations primarily alter the inclusion of alternatively spliced exons

Project description:Mutations primarily alter the inclusion of alternatively spliced exons

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Mutations primarily alter the inclusion of alternatively spliced exons

Project description:Systematic mutagenesis has revealed that synonymous, non-synonymous and intronic mutations frequently alter the inclusion levels of alternatively spliced exons, suggesting that altered splicing might be a common mechanism by which mutations cause disease. However, most exons expressed in any cell are highly-included in mature mRNAs. Here, by performing deep mutagenesis of highly-included exons and by analysing the association between sequence variation and exon inclusion across the genome, we report that mutations only very rarely alter the inclusion of highly-included exons. This is true for both exonic and intronic mutations as well as for perturbations in trans. Therefore, mutations that affect splicing are not evenly distributed across the genome but are focussed in and around alternatively spliced exons with intermediate inclusion levels. These results provide a resource for prioritising synonymous and other variants as disease-causing mutations.

2020-06-29 | GSE151942 | GEO

Gene expression profiling of Capan-1 and Pt45P1 cells treated or not with alternatively spliced tissue factor (asTF)

Project description:The effects of alternatively spliced tissue factor (asTF) were measured by gene expression profiling of Capan-1 and Pt45P1 cells.

2013-04-10 | GSE45928 | GEO

Heterogeneous Expression of Alternatively Spliced lncRNA mediates Vascular Smooth Cell Plasticity

Project description:Heterogeneous Expression of Alternatively Spliced lncRNA mediates Vascular Smooth Cell Plasticity

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Gene expression profiling of Capan-1 and Pt45P1 cells treated or not with alternatively spliced tissue factor (asTF)

Project description:The effects of alternatively spliced tissue factor (asTF) were measured by gene expression profiling of Capan-1 and Pt45P1 cells. 4 samples: Capan-1 cells +/- asTF, Pt45P1 cells +/- asTF.

2013-04-10 | E-GEOD-45928 | biostudies-arrayexpress

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