ArticleOncogene2016
Onco-exaptation of an endogenous retroviral LTR drives IRF5 expression in Hodgkin lymphoma.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 118 citations in OpenAlex.
- Endogenous retrovirus control of calbindin is essential for human early embryogenesis.Science advances · 2026Article
- Transposable Element Activation: A Hallmark of Cancer.Cancer discovery · 2026Review
- DICER1-related tumour predisposition mutations increase 3p-miRNA function and HERVH activity.Nature communications · 2026Article
- CDK9 Inhibition with enitociclib reveals influence on HERV and LINE RNA abundances in whole blood, T-, and B-Cell lines.BMC medical genomics · 2026Article
- Oncogenic role of ERV with therapeutic potential.Frontiers in immunology · 2026Review
- How Oncovirus Affects Drug Resistance in Cancer Cells.Recent patents on anti-cancer drug discovery · 2026Review
- Endogenous retroviruses in aging and cancer: from genomic defense to oncogenic activation.Mobile DNA · 2025Review
- Enhancer activation from transposable elements in extrachromosomal DNA.Nature cell biology · 2025Article
- Transcriptional and post-transcriptional regulation of transposable elements and their roles in development and disease.Nature reviews. Molecular cell biology · 2025Review
- Enhancer activation from transposable elements in extrachromosomal DNA.bioRxiv : the preprint server for biology · 2025Article
- Immune System-Tumor Crosstalk Under Microgravity: Mechanistic Insights, Challenges, and Translational Perspectives.Cancers · 2025Review
- Identification of cell-type-specific, transcriptionally active transposable elements using long-read RNA-sequencing data-based comprehensive annotation.Genomics & informatics · 2025Article
- Co-option of an endogenous retrovirus (LTR7-HERVH) in early human embryogenesis: becoming useful and going unnoticed.Mobile DNA · 2025Review
- Article
- Charting the regulatory landscape of TP53 on transposable elements in cancer.Genome research · 2025Article
- Retroelement co-option disrupts the cancer transcriptional programme.Genome medicine · 2025Article
- Transposable elements as genome regulators in normal and malignant haematopoiesis.Blood cancer journal · 2025Review
- Transposable elements may enhance antiviral resistance in HIV-1 elite controllers.Genome biology · 2025Article
- Stratification system with dual human endogenous retroviruses for predicting immunotherapy efficacy in metastatic clear-cell renal cell carcinoma.Journal for immunotherapy of cancer · 2025Article
- Endogenous retroelements in hematological malignancies: From epigenetic dysregulation to therapeutic targeting.American journal of hematology · 2025Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor interferon regulatory factor 5 (IRF5) is upregulated in Hodgkin lymphoma (HL) and is a key regulator of the aberrant transcriptome characteristic of this disease. Here we show that IRF5 upregulation in HL is driven by transcriptional activation of a normally dormant endogenous retroviral LOR1a long terminal repeat (LTR) upstream of IRF5. Specifically, through screening of RNA-sequencing libraries, we detected LTR-IRF5 chimeric transcripts in multiple HL cell lines but not in normal B-cell controls. In HL, the LTR was in an open and hypomethylated epigenetic state, and we further show the LTR is the site of transcriptional initiation. Among HL cell lines, usage of the LTR promoter strongly correlates with overall levels of IRF5 mRNA and protein, indicating that LTR transcriptional awakening is a major contributor to IRF5 upregulation in HL. Taken together, oncogenic IRF5 overexpression in HL is the result of a specific LTR transcriptional activation. We propose that such LTR derepression is a distinct mechanism of oncogene activation ('onco-exaptation'), and that such a mechanism warrants further investigation in molecular and cancer research.
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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.