An LTR retrotransposon‐derived lncRNA interacts with RNF169 to promote homologous recombination
Open accessAbstract
LTR retrotransposons are abundant repetitive elements in the human genome, but their functions remain poorly understood. Here, we report the function and regulatory mechanism of an ERV-9 LTR retrotransposon-derived lncRNA called p53-regulated lncRNA for homologous recombination (HR) repair 1 (PRLH1) in human cells. PRLH1 is highly expressed in p53-mutated hepatocellular carcinoma (HCC) samples and promotes cell proliferation in p53-mutated HCC cells, and its transcription is promoted by NF-Y and suppressed by p53. Mechanistically, PRLH1 specifically binds to an uncharacterized domain of RNF169 through two GCUUCA boxes in its 5' terminal region to form a DNA repair complex that supplants 53BP1 at double-strand break (DSB) sites and then promotes the initiation of HR repair. Notably, PRLH1 is essential for the stabilization of RNF169, acting as an RNA platform to recruit and assemble HR protein factors. This study characterizes PRLH1 as a novel HR-promoting factor and provides new insights into the function and mechanism of LTR retrotransposon-derived lncRNAs.
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The genes with promoter DNA hypomethylation include AFP, several HCC-related lncRNAs (LINC01419, LINC02163, LINC02835), and tumor-associated antigens such as the MAGE gene family.
“These genes included AFP, a diagnostic marker for HCC, several HCC-related lncRNAs (LINC01419, LINC02163, and LINC02835), and tumor-associated antigens such as the MAGE gene family35–37.”
From Multi-omic analysis of hepatocellular carcinoma reveals aberrant cis-regulatory changes and dysregulated retrotransposons with prognostic potential (2025) · cites this paper as [37]
The section “PRLH1 is an ERV9 LTR lncRNA regulated by p53” (page unavailable) identifies LINC01419 as a lncRNA upregulated in HCC. The copy does not establish promoter DNA hypomethylation for it or identify AFP, LINC02163, LINC02835, or the MAGE family as genes with hypomethylated promoters. A discussion of possible CpG methylation at the PRLH1 promoter does not establish the claimed hypomethylation. (LLM, conf=0.86)
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- Authors
- Deng, B., Xu, W., Wang, Z., Liu, C., Lin, P., Li, B., Huang, Q., Yang, J., Zhou, H., & Qu, L.
- Affiliations
- Sun Yat-sen University (CN)
- Corresponding author
- Yang, Jianhua
- Zhou, Hui
- Venue
- The EMBO Reports
- Published
- 2019-09-05
- Volume
- 20
- Issue
- 11
- Pages
- e47650-e47650
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC6832013
- OpenAlex
- W2971402088
- Cited by
- 40
- References
- 77
- Citations by year
- 2025: 5 · 2024: 9 · 2023: 9 · 2022: 5 · 2021: 7 · 2020: 4 · 2019: 1
- FWCI
- 1.34
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- EMBO Reports (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Science and Technology of the People's Republic of China (2017YFA0504400, 2011CB811300)
- National Natural Science Foundation of China (31471223, 31671349, 31770879)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
- Keywords
- LTR retrotransposons, long non-coding RNA, homologous recombination, DNA double-strand break repair, 53BP1, TP53 mutation, hepatocellular carcinoma, NF-Y, RNA-protein interactions, protein stabilization
- MeSH terms
- Tumor Suppressor p53-Binding Protein 1, Base Sequence, Binding Sites, DNA Repair, Epistasis, Genetic, Gene Expression Regulation, Carcinoma, Hepatocellular, Humans, Liver Neoplasms, Models, Biological, Promoter Regions, Genetic, Protein Binding, Tumor Suppressor Protein p53, Retroelements, Terminal Repeat Sequences, CCAAT-Binding Factor, Ubiquitin-Protein Ligases, Cell Proliferation, DNA Breaks, Double-Stranded, Protein Stability, Homologous Recombination, RNA, Long Noncoding
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