A novel long noncoding RNA Linc-ASEN represses cellular senescence through multileveled reduction of p21 expression
DC Field | Value | Language |
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dc.contributor.author | Lee, Hyung Chul | - |
dc.contributor.author | Kang, Donghee | - |
dc.contributor.author | Han, Namshik | - |
dc.contributor.author | Lee, Yerim | - |
dc.contributor.author | Hwang, Hyun Jung | - |
dc.contributor.author | Lee, Sat-Byol | - |
dc.contributor.author | You, Jueng Soo | - |
dc.contributor.author | Min, Byung Soh | - |
dc.contributor.author | Park, Heon Joo | - |
dc.contributor.author | Ko, Young-Gyu | - |
dc.contributor.author | Gorospe, Myriam | - |
dc.contributor.author | Lee, Jae-Seon | - |
dc.date.accessioned | 2021-08-30T22:27:38Z | - |
dc.date.available | 2021-08-30T22:27:38Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2020-06 | - |
dc.identifier.issn | 1350-9047 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/55560 | - |
dc.description.abstract | 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. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.subject | MESSENGER-RNAS | - |
dc.subject | DECAY | - |
dc.subject | GENE | - |
dc.subject | UPF1 | - |
dc.subject | CHROMATIN | - |
dc.subject | CANCER | - |
dc.subject | ROLES | - |
dc.subject | MECHANISMS | - |
dc.subject | PRINCIPLES | - |
dc.subject | MACHINERY | - |
dc.title | A novel long noncoding RNA Linc-ASEN represses cellular senescence through multileveled reduction of p21 expression | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Ko, Young-Gyu | - |
dc.identifier.doi | 10.1038/s41418-019-0467-6 | - |
dc.identifier.scopusid | 2-s2.0-85076581255 | - |
dc.identifier.wosid | 000534930000008 | - |
dc.identifier.bibliographicCitation | CELL DEATH AND DIFFERENTIATION, v.27, no.6, pp.1844 - 1861 | - |
dc.relation.isPartOf | CELL DEATH AND DIFFERENTIATION | - |
dc.citation.title | CELL DEATH AND DIFFERENTIATION | - |
dc.citation.volume | 27 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 1844 | - |
dc.citation.endPage | 1861 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | MESSENGER-RNAS | - |
dc.subject.keywordPlus | DECAY | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | UPF1 | - |
dc.subject.keywordPlus | CHROMATIN | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | ROLES | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | PRINCIPLES | - |
dc.subject.keywordPlus | MACHINERY | - |
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