ArticleScientific reports2016
Epigenetic inactivation of the CpG demethylase TET1 as a DNA methylation feedback loop in human cancers.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 126 citations in OpenAlex.
- Regulatory function of ten‑eleven translocation‑2 in transcriptional mechanisms of demethylated myeloma cells.Molecular medicine reports · 2026Article
- Epigenetics in lung cancer precision medicine: from bench to bedside-a narrative review.Translational lung cancer research · 2026Review
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- Epigenetic mechanisms of Parkinson's disease and potential epigenetic-based therapeutics.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- 5-Hydroxymethylcytosine: a key epigenetic mark in cancer and chemotherapy response.Epigenetics & chromatin · 2025Review
- The Bermuda Triangle of paediatric brain cancers: epigenetics, developmental timing window and cell of origin.Cancer metastasis reviews · 2025Review
- TET1 functions as a tumor suppressor in lung adenocarcinoma through epigenetic remodeling and immune modulation.Epigenetics & chromatin · 2025Article
- Long interspersed nuclear element 1 methylation in non-small cell lung cancer: implications for diagnosis, prognosis, and therapeutic targeting.Cell communication and signaling : CCS · 2025Review
- Mesenchymal stem cells modulate breast cancer progression through their secretome by downregulating ten-eleven translocation 1.Scientific reports · 2025Article
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- Regulatory mechanisms of m6A RNA methylation in esophageal cancer: a comprehensive review.Frontiers in genetics · 2025Review
- Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma and its Clinical Implications in Systemic Chemotherapy.International journal of medical sciences · 2025Review
- The role of circulating tumor DNA in gynecological cancer management.Frontiers in oncology · 2025Review
- Review
- Selective Estrogen Receptor Modulators' (SERMs) Influence onInternational journal of molecular sciences · 2024Article
- Prediction of the binding mechanism of a selective DNA methyltransferase 3A inhibitor by molecular simulation.Scientific reports · 2024Article
- The regulation of plasma gelsolin by DNA methylation in ovarian cancer chemo-resistance.Journal of ovarian research · 2024Article
- Pharmacogenomic and epigenomic approaches to untangle the enigma of IL-10 blockade in oncology.Expert reviews in molecular medicine · 2024Review
- TET enzyme driven epigenetic reprogramming in early embryos and its implication on long-term health.Frontiers in cell and developmental biology · 2024Review
- A Systematic Review of Epigenetics of Endometriosis.F&S reviews · 2024Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Promoter CpG methylation is a fundamental regulatory process of gene expression. TET proteins are active CpG demethylases converting 5-methylcytosine to 5-hydroxymethylcytosine, with loss of 5 hmC as an epigenetic hallmark of cancers, indicating critical roles of TET proteins in epigenetic tumorigenesis. Through analysis of tumor methylomes, we discovered TET1 as a methylated target, and further confirmed its frequent downregulation/methylation in cell lines and primary tumors of multiple carcinomas and lymphomas, including nasopharyngeal, esophageal, gastric, colorectal, renal, breast and cervical carcinomas, as well as non-Hodgkin, Hodgkin and nasal natural killer/T-cell lymphomas, although all three TET family genes are ubiquitously expressed in normal tissues. Ectopic expression of TET1 catalytic domain suppressed colony formation and induced apoptosis of tumor cells of multiple tissue types, supporting its role as a broad bona fide tumor suppressor. Furthermore, TET1 catalytic domain possessed demethylase activity in cancer cells, being able to inhibit the CpG methylation of tumor suppressor gene (TSG) promoters and reactivate their expression, such as SLIT2, ZNF382 and HOXA9. As only infrequent mutations of TET1 have been reported, compared to TET2, epigenetic silencing therefore appears to be the dominant mechanism for TET1 inactivation in cancers, which also forms a feedback loop of CpG methylation during tumorigenesis.
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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.