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Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIRP-seq]

ABSTRACT: Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIRP-seq]

PROVIDER: PRJNA527315 | ENA |

REPOSITORIES: ENA

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	SRR8735108.fastq.gz	Fastqsanger.gz

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Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIRP-seq]

Project description:Long noncoding RNAs regulating diverse cellular processes implicate in many diseases. Here, we report the identification of a novel long intergenic noncoding RNA, Linc-ASEN, expressed in prematurely senescent cells, that associates with UPF1 and represses cellular senescence by reducing p21 production transcriptionally and post-transcriptionally. The Linc-ASEN-UPF1 complex suppressed p21 transcription by recruiting Polycomb Repressive Complex 1 (PRC1) and PRC2 to the p21 locus, and thereby preventing binding of the transcriptional activator p53 on the p21 promoter. Moreover, the Linc-ASEN-UPF1 complex repressed p21 expression post-transcriptionally by lowering p21 mRNA stability in association with DCP1A. Accordingly, Linc-ASEN levels were found inversely correlated with p21 mRNA levels in tumor tissues from patient-derived xenograft mice, in various human cancer tissues, and in aged mice tissues. Our studies reveal that Linc-ASEN prevents cellular senescence by reducing the transcription and stability of p21 mRNA in concert with UPF1, and suggest that Linc-ASEN might be a potential therapeutic target in processes influenced by senescence, including cancer.

2019-09-24 | GSE128396 | GEO

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [RNA-seq]

2019-09-24 | GSE128395 | GEO

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIP-seq]

2019-09-24 | GSE128397 | GEO

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence

Project description:Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence

| PRJNA527314 | ENA

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [RNA-seq]

Project description:Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [RNA-seq]

| PRJNA527316 | ENA

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIP-seq]

Project description:Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIP-seq]

| PRJNA527317 | ENA

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence

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

2019-09-24 | GSE128398 | GEO

A novel long noncoding RNA Linc-ASEN represses cellular senescence through multileveled reduction of p21 expression.

Project description:Long noncoding RNAs (lncRNAs) regulating diverse cellular processes implicate in many diseases. However, the function of lncRNAs in cellular senescence remains largely unknown. Here we identify a novel long intergenic noncoding RNA Linc-ASEN expresses in prematurely senescent cells. We find that Linc-ASEN associates with UPF1 by RNA pulldown mass spectrometry analysis, and represses cellular senescence by reducing p21 production transcriptionally and posttranscriptionally. Mechanistically, the Linc-ASEN-UPF1 complex suppressed p21 transcription by recruiting Polycomb Repressive Complex 1 (PRC1) and PRC2 to the p21 locus, and thereby preventing binding of the transcriptional activator p53 on the p21 promoter through histone modification. In addition, the Linc-ASEN-UPF1 complex repressed p21 expression posttranscriptionally by enhancing p21 mRNA decay in association with DCP1A. Accordingly, Linc-ASEN levels were found to correlate inversely with p21 mRNA levels in tumors from patient-derived mouse xenograft, in various human cancer tissues, and in aged mice tissues. Our results reveal that Linc-ASEN prevents cellular senescence by reducing the transcription and stability of p21 mRNA in concert with UPF1, and suggest that Linc-ASEN might be a potential therapeutic target in processes influenced by senescence, including cancer.

| S-EPMC7244501 | biostudies-literature

In vivo characterization of Linc-p21 reveals functional cis-regulatory DNA elements

Project description:In vivo characterization of Linc-p21 reveals functional cis-regulatory DNA elements

| PRJNA297110 | ENA

TWIST1 methylation by SETD6 selectively antagonizes LINC-PINT expression in Glioblastoma multiforme

Project description:Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor among adults, which is characterized by high invasion, migration and proliferation abilities. One important process that contributes to the invasiveness of GBM is the epithelial to mesenchymal transition (EMT). EMT is regulated by a set of defined transcription factors which tightly regulate this process, among them is the basic helix-loop-helix family member, TWIST1. Here we show that TWIST1 is methylated on lysine-33 at chromatin by SETD6, a methyltransferase with expression levels correlating with poor survival in GBM patients. RNA-seq analysis in U251 GBM cells suggested that both SETD6 and TWIST1 regulate cell adhesion and migration processes. We further show that TWIST1 methylation attenuates the expression of the long-non-coding RNA, LINC-PINT, thereby suppressing EMT in GBM. Mechanistically, TWIST1 methylation represses the transcription of LINC-PINT by increasing the occupancy of EZH2 and the catalysis of the repressive H3K27me3 mark at the LINC-PINT locus. Under un-methylated conditions, TWIST1 dissociates from the LINC-PINT locus, allowing the expression of LINC-PINT which leads to increased cell adhesion and decreased cell migration. Together, our findings unravel a new mechanistic dimension for selective expression of LINC-PINT mediated by TWIST1 methylation.

2022-08-12 | PXD029361 | Pride

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