ArticleNature cell biology2015
Non-canonical NF-κB signalling and ETS1/2 cooperatively drive C250T mutant TERT promoter activation.
Article in Nature cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
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134 citing papers in PubMed, 205 citations in OpenAlex.
- The intersection of chemokine signaling with the hallmarks of cancer in glioblastoma.Journal of neuro-oncology · 2026Review
- Non-Telomeric Role of RAP1 in Facilitating NF-κB Activation and Driving Hepatocellular Carcinoma Progression.IUBMB life · 2026Article
- Dual TERT promoter mutations in glioblastoma, IDH-wildtype: a case report with preclinical investigations.Brain tumor pathology · 2026Article
- The transcription complex p52-ETS1 is essential for germinal center formation.Nature immunology · 2025Article
- A unique p52 NF-κB-ETS1 interaction ushers in a new paradigm of germinal center responses.Nature immunology · 2025Article
- NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025Review
- The -124C>T Mutation of theCurrent oncology (Toronto, Ont.) · 2025Article
- TLR4/NF-κB-mediated M1 macrophage polarization contributes to the promotive effects of ETS2 on ulcerative colitis.European journal of medical research · 2025Article
- Sarcopenia: Current Insights into Molecular Mechanisms, Diagnostics, and Emerging Interventional Approaches.International journal of molecular sciences · 2025Review
- The immortality mechanism of TERT promoter mutant cancers is self-reinforcing and reversible.Molecular cell · 2025Article
- Multi-omic analysis of SDHB-deficient pheochromocytomas and paragangliomas identifies metastasis and treatment-related molecular profiles.Nature communications · 2025Article
- Genetically Engineered Brain Organoids Recapitulate Spatial and Developmental States of Glioblastoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- BRAF-induced EHF Expression Affects TERT in Aggressive Papillary Thyroid Cancer.The Journal of clinical endocrinology and metabolism · 2025Article
- Article
- Mechanistic basis of atypical TERT promoter mutations.Nature communications · 2024Article
- Molecular Determinants for Photodynamic Therapy Resistance and Improved Photosensitizer Delivery in Glioma.International journal of molecular sciences · 2024Review
- TWEAK/Fn14 signalling driven super-enhancer reprogramming promotes pro-metastatic metabolic rewiring in triple-negative breast cancer.Nature communications · 2024Article
- Multi-omic analysis of SDHB-deficient pheochromocytomas and paragangliomas identifies metastasis and treatment-related molecular profiles.Research square · 2024Article
- IMPDH Inhibition Decreases TERT Expression and Synergizes the Cytotoxic Effect of Chemotherapeutic Agents in Glioblastoma Cells.International journal of molecular sciences · 2024Article
- Therapeutic targeting of PLK1 in TERT promoter-mutant hepatocellular carcinoma.Clinical and translational medicine · 2024Article
74 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
Transcriptional reactivation of TERT, the catalytic subunit of telomerase, is necessary for cancer progression in about 90% of human cancers. The recent discovery of two prevalent somatic mutations-C250T and C228T-in the TERT promoter in various cancers has provided insight into a plausible mechanism of TERT reactivation. Although the two hotspot mutations create a similar binding motif for E-twenty-six (ETS) transcription factors, we show that they are functionally distinct, in that the C250T unlike the C228T TERT promoter is driven by non-canonical NF-κB signalling. We demonstrate that binding of ETS to the mutant TERT promoter is insufficient in driving its transcription but this process requires non-canonical NF-κB signalling for stimulus responsiveness, sustained telomerase activity and hence cancer progression. Our findings highlight a previously unrecognized role of non-canonical NF-κB signalling in tumorigenesis and elucidate a fundamental mechanism for TERT reactivation in cancers, which if targeted could have immense therapeutic implications.
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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.