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

Authors
Lee, Hyung ChulKang, DongheeHan, NamshikLee, YerimHwang, Hyun JungLee, Sat-ByolYou, Jueng SooMin, Byung SohPark, Heon JooKo, Young-GyuGorospe, MyriamLee, Jae-Seon
Issue Date
6월-2020
Publisher
NATURE PUBLISHING GROUP
Citation
CELL DEATH AND DIFFERENTIATION, v.27, no.6, pp.1844 - 1861
Indexed
SCIE
SCOPUS
Journal Title
CELL DEATH AND DIFFERENTIATION
Volume
27
Number
6
Start Page
1844
End Page
1861
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/55560
DOI
10.1038/s41418-019-0467-6
ISSN
1350-9047
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.
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