ArticleNature2008
Epigenetic silencing of tumour suppressor gene p15 by its antisense RNA.
Article in Nature, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 458 papers, 3 of them syntheses that pooled it.
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Who cites it
458 citing papers in PubMed, 3 syntheses or guidelines pooled it, 801 citations in OpenAlex.
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- LINC00472 expression is regulated by promoter methylation and associated with disease-free survival in patients with grade 2 breast cancer.Breast cancer research and treatment · 2015Pooled it
- Prognostic and predictive values of long non-coding RNA LINC00472 in breast cancer.Oncotarget · 2015Pooled it
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- Mechanisms linking cytoplasmic decay of translation-defective mRNA to transcriptional adaptation.Science (New York, N.Y.) · 2026Article
- Identification of circular RNAs as biomarkers for pupal age estimation and postmortem interval in forensically important Sarcophaga peregrina (Diptera: Sarcophagidae).International journal of legal medicine · 2025Article
- Cancer driver topologically associated domains identify oncogenic and tumor-suppressive lncRNAs.Genome research · 2025Article
- Mechanism of expression regulation of head-to-head overlapping protein-coding genes INO80E and HIRIP3.Communications biology · 2025Article
- A novel mechanism by which c-MYC is aberrantly activated by epigenetic silencing of its antisense lncRNA in colon cancer.Frontiers in genetics · 2025Article
- Gene regulation by convergent promoters.Nature genetics · 2025Article
- The oncogenic lncRNA MIR503HG suppresses cellular senescence counteracting supraphysiological androgen treatment in prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- The seeds of its regulation: Natural antisense transcripts as single-gene control switches in neurodegenerative disorders.Ageing research reviews · 2024Review
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- SH-SY5Y human neuronal cells with mutations of theBiochemistry and biophysics reports · 2024Article
- The expression and function of long noncoding RNAs in hepatocellular carcinoma.Cancer innovation · 2023Review
- Identification cloning and functional analysis of novel natural antisense lncRNA CFL1-AS1 in cattle.Epigenetics · 2023Article
- Broad-spectrum metastasis suppressing compounds and therapeutic uses thereof in human tumors.Scientific reports · 2023Article
- High-throughput identification of regulatory elements and functional assays to uncover susceptibility genes for nasopharyngeal carcinoma.American journal of human genetics · 2023Article
- Genome-wide association analysis identifies a susceptibility locus for sporadic vestibular schwannoma at 9p21.Brain : a journal of neurology · 2023Article
398 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Tumour suppressor genes (TSGs) inhibiting normal cellular growth are frequently silenced epigenetically in cancer. DNA methylation is commonly associated with TSG silencing, yet mutations in the DNA methylation initiation and recognition machinery in carcinogenesis are unknown. An intriguing possible mechanism for gene regulation involves widespread non-coding RNAs such as microRNA, Piwi-interacting RNA and antisense RNAs. Widespread sense-antisense transcripts have been systematically identified in mammalian cells, and global transcriptome analysis shows that up to 70% of transcripts have antisense partners and that perturbation of antisense RNA can alter the expression of the sense gene. For example, it has been shown that an antisense transcript not naturally occurring but induced by genetic mutation leads to gene silencing and DNA methylation, causing thalassaemia in a patient. Here we show that many TSGs have nearby antisense RNAs, and we focus on the role of one RNA in silencing p15, a cyclin-dependent kinase inhibitor implicated in leukaemia. We found an inverse relation between p15 antisense (p15AS) and p15 sense expression in leukaemia. A p15AS expression construct induced p15 silencing in cis and in trans through heterochromatin formation but not DNA methylation; the silencing persisted after p15AS was turned off, although methylation and heterochromatin inhibitors reversed this process. The p15AS-induced silencing was Dicer-independent. Expression of exogenous p15AS in mouse embryonic stem cells caused p15 silencing and increased growth, through heterochromatin formation, as well as DNA methylation after differentiation of the embryonic stem cells. Thus, natural antisense RNA may be a trigger for heterochromatin formation and DNA methylation in TSG silencing in tumorigenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.