ArticleJournal of virology2013
A novel function of RNAs arising from the long terminal repeat of human endogenous retrovirus 9 in cell cycle arrest.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Human endogenous retroviruses (HERVs) associated with glioblastoma risk and prognosis.Cancer gene therapy · 2025Article
- Viral influencers: deciphering the role of endogenous retroviral LTR12 repeats in cellular gene expression.Journal of virology · 2025Review
- Transposons disrupt genomic stability and trigger cancers.Frontiers in cellular and infection microbiology · 2025Review
- The role of transposable elements in aging and cancer.Biogerontology · 2023Review
- HERVs and Cancer-A Comprehensive Review of the Relationship of Human Endogenous Retroviruses and Human Cancers.Biomedicines · 2023Review
- Retroviral Antisense Transcripts and Genes: 33 Years after First Predicted, a Silent Retroviral Revolution?Viruses · 2021Review
- Ancient viral integrations in marsupials: a potential antiviral defence.Virus evolution · 2021Article
- The Sophisticated Transcriptional Response Governed by Transposable Elements in Human Health and Disease.International journal of molecular sciences · 2020Review
- Novel reference genes in colorectal cancer identify a distinct subset of high stage tumors and their associated histologically normal colonic tissues.BMC medical genetics · 2019Article
- Expressional activation and functional roles of human endogenous retroviruses in cancers.Reviews in medical virology · 2019Review
- The animal nuclear factor Y: an enigmatic and important heterotrimeric transcription factor.American journal of cancer research · 2018Review
- Epigenetic modifier drugs trigger widespread transcription of endogenous retroviruses.Nature genetics · 2017Article
- Transposable Elements in Human Cancer: Causes and Consequences of Deregulation.International journal of molecular sciences · 2017Review
- The sense behind retroviral anti-sense transcription.Virology journal · 2017Article
- Endogenous retroviral promoter exaptation in human cancer.Mobile DNA · 2016Review
- Comprehensive identification of genes driven by ERV9-LTRs reveals TNFRSF10B as a re-activatable mediator of testicular cancer cell death.Cell death and differentiation · 2016Article
- Detecting endogenous retrovirus-driven tissue-specific gene transcription.Genome biology and evolution · 2015Article
- The intertwining of transposable elements and non-coding RNAs.International journal of molecular sciences · 2013Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
The human genome contains approximately 50 copies of the replication-defective human endogenous retrovirus 9 (ERV-9) and thousands of copies of its solitary long term repeat (sLTR) element. While some sLTRs are located upstream of critical genes and have enhancer activity, other sLTRs are located within introns and may be transcribed as RNAs. We found that intronic RNAs arising from U3 sLTRs of ERV-9 were expressed as both sense (S) and antisense (AS) transcripts in all human cells tested but that expression levels differed in malignant versus nonmalignant cells. In nonmalignant cells, AS was expressed at higher levels than S and at higher levels than in malignant cells; in malignant cells, AS was expressed at amounts equivalent to those of S RNA. Critically, U3 AS RNA was found to physically bind to key transcription factors for cellular proliferation, including NF-Y, p53, and sp1, indicating that such RNA transcripts may function as decoy targets or traps for NF-Y and thus inhibit the growth of human cancer cells. Indeed, short U3 oligodeoxynucleotides (ODNs) based on these RNA sequences ably inhibited proliferation of cancer cell lines driven by cyclins B1/B2, the gene targets of NF-Y.
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Identifiers
What OpenQuestion holds
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.