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RRP1B is a Metastasis Modifier that Regulates the Transcriptome through mRNA Splicing

ABSTRACT: RRP1B is a Metastasis Modifier that Regulates the Transcriptome through mRNA Splicing

ORGANISM(S): Mus musculus

PROVIDER: GSE38669 | GEO | 2014/06/08

SECONDARY ACCESSION(S): PRJNA168458

REPOSITORIES: GEO

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RRP1B is a Metastasis Modifier that Regulates the Transcriptome through mRNA Splicing

Project description:RRP1B is a Metastasis Modifier that Regulates the Transcriptome through mRNA Splicing To assess the role of RRP1B in alternative mRNA splicing, we knocked down the expression of Rrp1b in the highly metastatic mouse mammary tumor cell line Mvt-1 using shRNA. Two control and two knockdown stable cell lines were selected for RNA-sequencing.

2014-06-08 | E-GEOD-38669 | biostudies-arrayexpress

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [ChIP-Seq]

Project description:The processing of RNAs by chromatin-associated proteins (CAPs) is highlighted by the latest findings. However, whether and how CAP-RNA interactions regulate cancer biology remain underdefined. Using modified fCLIP-seq technology, we show that, cancer metastasis-associated antigen 1 (MTA1), a well-known oncogenic chromatin modifier, binds bulk transcripts, preferentially at splicing-responsible motifs, influencing the abundance and alternative splicing (AS) of target transcripts, preferentially those encoding mitosis regulators. MTA1 orchestrates the fluctuant pre-mRNA AS kinetics of mitosis regulators, such as ATRX and MYBL2, during mitosis. MTA1 overexpression causes a defective mitotic arrest, leading to aberrant chromosome segregation, and CIN occurrence in cancer cells and clinical tumors, which eventually contributes to tumorigenesis. Hence, we present MTA1 as a pivotal RNA-binding CAP linked to mitosis control in tumorigenesis.

2020-07-17 | GSE123955 | GEO

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [fCLIP-Seq]

2020-07-17 | GSE123956 | GEO

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [Synchronized RNA-seq]

2020-07-17 | GSE123958 | GEO

RNA-binding chromatin modifier MTA1 regulates mitotic transition and tumorigenesis by orchestrating mitotic mRNA processing [Non-synchronized RNA-seq]

2020-07-17 | GSE123957 | GEO

LINC00266-1-encoded peptide regulates mRNA splicing

Project description:LINC00266-1-encoded peptide regulates mRNA splicing

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The epigenetic modifier EZH2 controls melanoma growth and metastasis through silencing of distinct tumour suppressors

Project description:Increased activity of the epigenetic modifier EZH2 has been associated with different cancers. However, evidence for a functional role of EZH2 in tumourigenesis in vivo remains poor, in particular in metastasising solid cancers. Here we reveal central roles of EZH2 in promoting growth and metastasis of cutaneous melanoma. In a melanoma mouse model, conditional Ezh2 ablation as much as treatment with the preclinical Ezh2 inhibitor GSK503 stabilises the disease through inhibition of growth and virtually abolishes metastases formation without affecting normal melanocyte biology. Comparably, in human melanoma cells, EZH2 inactivation impairs proliferation and invasiveness, accompanied by re-expression of tumour suppressors connected to increased patient survival. These EZH2 target genes suppress melanoma growth and prevent EMT / metastasis in vivo revealing the dual function of EZH2 in promoting tumour progression. Thus, EZH2-mediated epigenetic repression is highly relevant especially during advanced melanomagenesis, which makes EZH2 a promising target for novel melanoma therapies.

2014-11-12 | GSE63165 | GEO

LOC90024-encoded small protein SRSP regulates mRNA splicing

Project description:LOC90024-encoded small protein SRSP regulates mRNA splicing

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RRP1B is a metastasis modifier that regulates the expression of alternative mRNA isoforms through interactions with SRSF1.

Project description:RRP1B (ribosomal RNA processing 1 homolog B) was first identified as a metastasis susceptibility gene in breast cancer through its ability to modulate gene expression in a manner that can be used to accurately predict prognosis in breast cancer. However, the mechanism(s) by which RRP1B modulates gene expression is currently unclear. Many RRP1B binding candidates are involved in alternative splicing, a mechanism of gene expression regulation that is increasingly recognized to be involved in cancer progression and metastasis. One such target is SRSF1 (serine/arginine-rich splicing factor 1) (SF2/ASF, splicing factor 2/alternative splicing factor), an essential splicing regulator that also functions as an oncoprotein. Earlier studies demonstrated that splicing and transcription occur concurrently and are coupled processes. Given that RRP1B regulates transcriptional activity, we hypothesized that RRP1B also regulates the expression of alternative mRNA isoforms through its interaction with SRSF1. Interaction between RRP1B and SRSF1 was verified by coimmunoprecipitation and coimmunofluorescence. Treatment of cells with transcriptional inhibitors significantly increased this interaction, demonstrating that the association of these two proteins is transcriptionally regulated. To assess the role of RRP1B in the regulation of alternative isoform expression, RNA-sequencing data were generated from control and Rrp1b-knockdown cells. Knockdown of Rrp1b induced a significant change in isoform expression in over 600 genes compared with control cell lines. This was verified by quantitative reverse-transcription PCR using isoform-specific primers. Pathway enrichment analyses identified cell cycle and checkpoint regulation to be those most affected by Rrp1b knockdown. These data suggest that RRP1B suppresses metastatic progression by altering the transcriptome through its interaction with splicing regulators such as SRSF1.

| S-EPMC3925194 | biostudies-literature

An Alternative Splicing Switch Regulates Embryonic Stem Cell Pluripotency and Reprogramming

Project description:This SuperSeries is composed of the following subset Series: GSE30995: An Alternative Splicing Switch Regulates Embryonic Stem Cell Pluripotency and Reprogramming [RNA-Seq] GSE31006: An Alternative Splicing Switch Regulates Embryonic Stem Cell Pluripotency and Reprogramming [ChIP-Seq] GSE31007: An Alternative Splicing Switch Regulates Embryonic Stem Cell Pluripotency and Reprogramming [protein binding microarray] GSE31948: An Alternative Splicing Switch Regulates Embryonic Stem Cell Pluripotency and Reprogramming [AS microarray] Refer to individual Series

2011-09-14 | E-GEOD-30992 | biostudies-arrayexpress

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