ArticleNature communications2022
ARID1A loss derepresses a group of human endogenous retrovirus-H loci to modulate BRD4-dependent transcription.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Endogenous retrovirus control of calbindin is essential for human early embryogenesis.Science advances · 2026Article
- BRD4: From molecular understanding to therapeutics development.Molecular cell · 2026Review
- Analysis of HERV-K (HML2) Expression in Colorectal Cancer Samples.Epigenomes · 2026Article
- Viral mimicry acts as a tumor suppressor in colitis.Nature communications · 2026Article
- Organoid research: new concepts and new technologies.Burns & trauma · 2026Review
- Activation of endogenous retroviruses in tumor cells and their immunomodulatory mechanisms: from molecular basis to clinical translation.Frontiers in oncology · 2026Review
- HERVH-derived eRNA activates a super-enhancer-driven ALDH1A3/SAT1 axis to promote ferroptosis escape and pancreatic cancer development.Science advances · 2025Article
- Transcriptional and post-transcriptional regulation of transposable elements and their roles in development and disease.Nature reviews. Molecular cell biology · 2025Review
- Co-option of an endogenous retrovirus (LTR7-HERVH) in early human embryogenesis: becoming useful and going unnoticed.Mobile DNA · 2025Review
- Human endogenous retroviruses (HERVs) associated with glioblastoma risk and prognosis.Cancer gene therapy · 2025Article
- Targeting HPV for the prevention, diagnosis, and treatment of cervical cancer.Journal of molecular cell biology · 2025Review
- Chromatin remodeling and cancer: the critical influence of the SWI/SNF complex.Epigenetics & chromatin · 2025Review
- HERV Modulation in Colorectal Carcinoma Patients: A Snapshot of Endogenous Retroviral Transcriptome.Journal of medical virology · 2025Article
- Reducing batch effects in single cell chromatin accessibility measurements by pooled transposition with MULTI-ATAC.bioRxiv : the preprint server for biology · 2025Article
- FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy.Nature communications · 2025Article
- The virome composition of respiratory tract changes in school-aged children with Mycoplasma pneumoniae infection.Virology journal · 2025Article
- ARID1A in Gynecologic Precancers and Cancers.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer.Science advances · 2024Article
- Towards targeting transposable elements for cancer therapy.Nature reviews. Cancer · 2024Review
- Transcriptional pausing induced by ionizing radiation enables the acquisition of radioresistance in nasopharyngeal carcinoma.Journal of molecular cell biology · 2024Article
Corrections and comments
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transposable elements (TEs) through evolutionary exaptation have become an integral part of the human genome, offering ample regulatory sequences and shaping chromatin 3D architecture. While the functional impacts of TE-derived sequences on early embryogenesis have been recognized, their roles in malignancy are only starting to emerge. Here we show that many TEs, especially the pluripotency-related human endogenous retrovirus H (HERVH), are abnormally activated in colorectal cancer (CRC) samples. Transcriptional upregulation of HERVH is associated with mutations of several tumor suppressors, particularly ARID1A. Knockout of ARID1A in CRC cells leads to increased transcription at several HERVH loci, which involves compensatory contribution by ARID1B. Suppression of HERVH in CRC cells and patient-derived organoids impairs tumor growth. Mechanistically, HERVH transcripts colocalize with nuclear BRD4 foci, modulating their dynamics and co-regulating many target genes. Altogether, we uncover a critical role for ARID1A in restraining HERVH, whose abnormal activation can promote tumorigenesis by stimulating BRD4-dependent transcription.
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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.