ArticleThe Journal of clinical investigation2020
Genomic and epigenomic EBF1 alterations modulate TERT expression in gastric cancer.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- EBF1 Regulates Cardiac Development Through Fibroblast to Myocyte Signaling.Journal of cardiovascular development and disease · 2026Article
- Novel Genetic Risk Loci for Pancreatic Ductal Adenocarcinoma Identified in a Genome-wide Study of African Ancestry Individuals.medRxiv : the preprint server for health sciences · 2026Article
- Multiscale characterization of an inflammatory macrophage state associated with an air pollutant-prioritized prognostic signature in gastric cancer.Frontiers in immunology · 2026Article
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- Article
- Advances in Research on the B-Lineage Transcription Factor EBF1 in Solid Tumors.International journal of molecular sciences · 2025Review
- Non-local modeling of enhancer-promoter interactions, a correspondence on "LOCO-EPI: Leave-one-chromosome-out (LOCO) as a benchmarking paradigm for deep learning based prediction of enhancer-promoter interactions".Applied intelligence (Dordrecht, Netherlands) · 2025Article
- Telomeres, telomerase, and cancer: mechanisms, biomarkers, and therapeutics.Experimental hematology & oncology · 2025Review
- Effect of SNORD113-3/ADAR2 on glycolipid metabolism in glioblastoma via A-to-I editing of PHKA2.Cellular & molecular biology letters · 2025Article
- Identification of the EBF1/ETS2/KLF2-miR-126-Gene Feed-Forward Loop in Breast Carcinogenesis and Stemness.International journal of molecular sciences · 2025Article
- Epigenetic Biomarkers and the Wnt/β-Catenin Pathway in Opisthorchis viverrini-associated Cholangiocarcinoma: A Scoping Review on Therapeutic Opportunities.PLoS neglected tropical diseases · 2024Article
- Machine learning identifies activation of RUNX/AP-1 as drivers of mesenchymal and fibrotic regulatory programs in gastric cancer.Genome research · 2024Article
- MicroRNAs provide negative feedback and stability in gene regulatory network models of cell-state transitions.Frontiers in epigenetics and epigenomics · 2024Article
- CamoTSS: analysis of alternative transcription start sites for cellular phenotypes and regulatory patterns from 5' scRNA-seq data.Nature communications · 2023Article
- HOXA5 is a key regulator of class 3 semaphorins expression in the synovium of rheumatoid arthritis patients.Rheumatology (Oxford, England) · 2023Article
- ZNF521/EBF1 axis regulates AKR1B1 to promote the proliferation, migration, and invasion of gastric cancer cells.The Kaohsiung journal of medical sciences · 2023Article
- Chromatin and noncoding RNA-mediated mechanisms of gastric tumorigenesis.Experimental & molecular medicine · 2023Review
- EBF1 promotes triple-negative breast cancer progression by surveillance of the HIF1α pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Reduced IRF4 expression promotes lytic phenotype in Type 2 EBV-infected B cells.PLoS pathogens · 2022Article
- Ecdysoneless Protein Regulates Viral and Cellular mRNA Splicing to Promote Cervical Oncogenesis.Molecular cancer research : MCR · 2022Article
Corrections and comments
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Authors and funding
46 authors at 13 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcriptional reactivation of telomerase catalytic subunit (TERT) is a frequent hallmark of cancer, occurring in 90% of human malignancies. However, specific mechanisms driving TERT reactivation remain obscure for many tumor types and in particular gastric cancer (GC), a leading cause of global cancer mortality. Here, through comprehensive genomic and epigenomic analysis of primary GCs and GC cell lines, we identified the transcription factor early B cell factor 1 (EBF1) as a TERT transcriptional repressor and inactivation of EBF1 function as a major cause of TERT upregulation. Abolishment of EBF1 function occurs through 3 distinct (epi)genomic mechanisms. First, EBF1 is epigenetically silenced via DNA methyltransferase, polycomb-repressive complex 2 (PRC2), and histone deacetylase activity in GCs. Second, recurrent, somatic, and heterozygous EBF1 DNA-binding domain mutations result in the production of dominant-negative EBF1 isoforms. Third, more rarely, genomic deletions and rearrangements proximal to the TERT promoter remobilize or abolish EBF1-binding sites, derepressing TERT and leading to high TERT expression. EBF1 is also functionally required for various malignant phenotypes in vitro and in vivo, highlighting its importance for GC development. These results indicate that multimodal genomic and epigenomic alterations underpin TERT reactivation in GC, converging on transcriptional repressors such as EBF1.
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