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

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

PROVIDER: PRJNA527317 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8735109.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]

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

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

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

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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 [ChIRP-seq]

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

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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

Protein-protein interactions of p21 in MCF7 cells during cellular senescence

Project description:A mass spectrometry-based proteomics analysis was performed to study the protein binders of p21 in MCF7 cells during the progression and maintenance of cellular senescence.

2024-06-02 | PXD042908 | Pride

Rack1 is Essential for Corticogenesis by Preventing P21-Dependent Senescence in Neural Stem Cells

Project description:Normal neurodevelopment relies on intricate signaling pathways that balance neural stem cell (NSC) self-renewal, maturation and survival. Disruptions lead to neurodevelopmental disorders including microcephaly. Here, we implicate the inhibition of NSC senescence as a mechanism underlying neurogenesis and corticogenesis. We report that the receptor for activated C kinase (Rack1), a family member of WD40-repeat (WDR) proteins, is highly enriched in NSCs. Deletion of Rack1 in developing cortical progenitors leads to a microcephaly phenotype. Strikingly, the absence of Rack1 decreases neurogenesis and promotes a cellular senescence phenotype in NSCs. Mechanistically, the senescence-related p21 signaling pathway is dramatically activated in Rack1-null NSCs, and removal of p21 significantly rescues the Rack1-knockout phenotype in vivo. Finally, Rack1 directly interacts with Smad3 to suppress the activation of TGF-β/Smad signaling pathway, which plays a critical role in p21-mediated senescence. Our data implicate Rack1-driven inhibition of p21-induced NSC senescence as a critical mechanism behind normal cortical development.

2021-08-09 | PXD027798 |

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