PreprintCited by 1,040Epigenetics and DNA MethylationGenomics and Chromatin DynamicsCancer-related gene regulation

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Role of TET enzymes in DNA methylation, development, and cancer

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Rasmussen, Kasper Dindler, Helin, Kristian·2016·Genes & Development

DOI 10.1101/gad.276568.115PMC PMC4826392

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Abstract

The pattern of DNA methylation at cytosine bases in the genome is tightly linked to gene expression, and DNA methylation abnormalities are often observed in diseases. The ten eleven translocation (TET) enzymes oxidize 5-methylcytosines (5mCs) and promote locus-specific reversal of DNA methylation. TET genes, and especially TET2 , are frequently mutated in various cancers, but how the TET proteins contribute to prevent the onset and maintenance of these malignancies is largely unknown. Here, we highlight recent advances in understanding the physiological function of the TET proteins and their role in regulating DNA methylation and transcription. In addition, we discuss some of the key outstanding questions in the field.

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Figure 1. Domain structure of TET proteins. The C-terminal core catalytic domain shared by all TET enzymes consists of the DSBH domain, a cysteine-rich (Cys) domain, and binding sites for the Fe(II) and 2-OG cofactors. The DSBH domain contains a large low-complexity region of unknown function. TET1 and TET3 have an N-terminal CXXC domain that can bind directly to DNA and facilitate recruitment to genomic target sites.CC BY-NC · PubMed Central

Figure 2. Pathways of DNA demethylation mediated by TET enzymes. (A) Model of passive replication-dependent DNA demethylation. The diagrams illustrate the two opposite fates of a hemihydroxymethylated CpG dinucleotide through two rounds of DNA replication. The left panel shows the replication-dependent DNA demethylation, in which DNA methylation is lost on the DNA strand opposite to 5hmC. The right panel shows the reverse outcome, in which maintenance of DNA methylation is achieved by DNMT1 in complex with UHRF1/2 or DNMT3A/B. The relative extent of these two opposing outcomes of 5hmC deposition in vivo remains to be determined and is likely influenced by global as well as locus-specific factors. In both cases, newly replicated DNA dilutes 5hmC during cell division. (B) Model of active DNA demethylation by a TET/TDG (thymine–DNA–glycosylase)/BER (base excision repair)-dependent pathway. A cytosine base can be methylated by the DNA methylation machinery (DNMT1 or DNMT3A/B) to form 5mC, which in turn can be iteratively oxidized by TET enzymes to produce 5hmC, 5fC, and 5caC. TDG then recognizes 5fC and 5caC, and the oxidized cytosine base is excised. This yields an abasic site that is repaired by BER and results in restoration of the unmodified cytosine state. Additional pathways of active DNA demethylation have been suggested (for review, see Wu and Zhang 2014). (SAH) S-adenosyl-homocysteine; (SAM) S-adenosyl-methionine.CC BY-NC · PubMed Central

Figure 3. The dynamics of TET-mediated cytosine oxidation and its impact on DNA methylation patterns on regulatory elements in vivo. (A) Diagram illustrating the relative abundance of cytosines in the genome with “stable” levels of modifications as well as the small “transient” fractions that undergo rapid turnover and removal by active DNA demethylation processes. The stable levels of genomic 5caC have not been experimentally determined, as they are often under the detection limit. (B) Model illustrating the dual role of TET enzymes. The rate constant of TET enzymes to produce 5hmC from 5mC is fast, whereas the rate constants for further oxidation to 5fC and 5caC are considerably slower. On a majority of TET target sites, 5mC is oxidized and persists as “stable” 5hmC, likely due to low TET residence time (“stalling TET modification”). On a minority of sites, preferably located in open chromatin associated with regulatory elements, 5mC is oxidized iteratively to 5fC and 5caC and results in net DNA demethylation by the TET/TDG/BER pathway (“processive TET modification”). (C) Model illustrating the impact of loss of TET protein function on different regulatory elements. The protection of active and inactive CpG island promoters by the TET proteins is only one of several mechanisms by which they are protected against ectopic DNA methylation. In contrast, distal regulatory elements such as active enhancers are vulnerable to aberrant DNMT activity and become DNA hypermethylated upon loss of TET activity. (PcG) Polycomb group.CC BY-NC · PubMed Central

Figure 4. Illustration of the mutational landscape of TET2 in hematological diseases. A somatic mutation in TET2 results in premalignant hematopoiesis and clonal expansion. Additional oncogenic events cooperate with the initial TET2 mutation to drive the onset of a wide variety of hematopoietic malignancies. The frequencies of TET2 mutations in the different patient groups are indicated (for review, see Scourzic et al. 2015).CC BY-NC · PubMed Central

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“Thus, it was remarkable when ten eleven translocation protein 1 (TET1) was discovered and shown to be able to modify methylcytosine and potentially erase DNAmethylation (Tahiliani et al. 2009).”
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“Second, TET2 mutations are frequently observed in aged healthy individuals with clonal hematopoiesis and increase the propensity to develop hematopoieticmalignancies (Busque et al. 2012; Genovese et al. 2014; Jaiswal et al. 2014; Xie et al. 2014).”
Background
Tet proteins can convert 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine
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“6-fold) substrates compared with the initial oxidation reaction of 5mC (Ito et al. 2011; Hu et al. 2015).”
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Oncometabolite 2-Hydroxyglutarate Is a Competitive Inhibitor of α-Ketoglutarate-Dependent Dioxygenases
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“Subsequent to the discovery of oxidized 5mC bases, it was demonstrated that TDG has no effect on 5hmC but shows robust recruitment and in vitro catalytic activity toward 5fC and 5caC (He et al. 2011; Maiti and Drohat 2011; Spruijt et al. 2013).”
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“By comparison, the products of further TET-mediated oxidation, 5fC and 5caC, are observed at ∼10-fold to 100-fold lower levels than 5hmC and often close to or under the detection limit (Kriaucionis and Heintz 2009; Globisch et al. 2010; Szwagierczak et al. 2010; He et al. 2011; Ito et al. 2011; Pfaffeneder et al. 2011…”
Background

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Background
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Background
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“3,76,92,93,94 We found that Tet methylcytosine dioxygenase 1 (TET1), a potent epigenetic factor involved in DNA methylation, 95,91 plays a role in innate immunity gene-regulated events during direct cardiac reprogramming.”
Deficiency of T follicular helper cell Tet3 DNA demethylation inhibits pathogenic IgG2c class switching and chronic GVHD
Zaiken, M. C., Jin, S., McDonald-Hyman, C. S., Hartigan, C. R., Sage, P. T., Hippen, K. L., Koehn, B. H., Panoskaltsis‐Mortari, A., Riddle, M. J., Eide, C. R., et al. (2025) · Blood · doi:10.1182/blood.2024025036 · Cited by 8
DNA Methylation in Periodontal Disease: A Focus on Folate, Folic Acid, Mitochondria, and Dietary Intervention
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“In addition to passive demethylation, DNA can undergo active demethylation by the ten-eleven translocation (TET) proteins TET1-3, with the assistance of thymine DNA glycosylase, a base excision DNA repair enzyme [7].”
Epigenetics for Clinicians from the Perspective of Pediatric Rheumatic Diseases
Akbaba, T. H., Sağ, E., Balcı‐Peynircioğlu, B., & Özen, S. (2020) · Current Rheumatology Reports · doi:10.1007/s11926-020-00912-9 · Cited by 8
TET3 dioxygenase modulates gene conversion at the avian immunoglobulin variable region via demethylation of non‐CpG sites in pseudogene templates
Takamura, N., Seo, H., & Ohta, K. (2021) · Genes to Cells · doi:10.1111/gtc.12828 · Cited by 8
“TET proteins are reportedly important in the maintenance of cell pluripotency, differentiation, neuronal functions and cancer development (Rasmussen & Helin, 2016; Wu & Zhang, 2017).”
BackgroundResult
Common mechanisms cannot explain time- and dose-dependent DNA methylation changes in earthworms exposed to cadmium
Aigner, G. P., Pittl, V., Fiechtner, B., Egger, B., Šrut, M., & Höckner, M. (2021) · The Science of The Total Environment · doi:10.1016/j.scitotenv.2021.151468 · Cited by 8
DNA Methylation and Detoxification in the Earthworm Lumbricus terrestris Exposed to Cadmium and the DNA Demethylation Agent 5-aza-2′-deoxycytidine
Aigner, G. P., Nenning, P., Fiechtner, B., Šrut, M., & Höckner, M. (2022) · Toxics · doi:10.3390/toxics10020100 · Cited by 8
“TET enzymes iteratively oxidize 5mC to 5-hydroxymethylcytosine (5hmC), 5hmC to 5-formylcytosine (5fC) and 5fC to 5-carboxylcytosine (5caC) [27].”
Background
Locus-Specific Enrichment Analysis of 5-Hydroxymethylcytosine Reveals Novel Genes Associated with Breast Carcinogenesis
Ramasamy, D., Rao, A. K. D. M., Meenakumari, B., Arvinden, V. R., Sundersingh, S., Veluswami, S., Rajkumar, T., & Mani, S. (2022) · Cells · doi:10.3390/cells11192939 · Cited by 8
VGLL4-TEAD1 promotes vascular smooth muscle cell differentiation from human pluripotent stem cells via TET2
Wang, Z., Quan, Y., Hu, M., Yubin, X., Chen, Y., Jin, P., Ma, J., Chen, X., Fan, J., Fan, X., et al. (2023) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2023.01.005 · Cited by 8
Global Patterns of Methylation in Sézary Syndrome Provide Insight into the Role of Epigenetics in Cutaneous T-Cell Lymphoma
Whittaker, S. J. (2016) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2016.05.114 · Cited by 8
Comparison of DNA and RNA substrate effects on TET2 structure
Leddin, E. M., & Cisneros, G. A. (2019) · Advances in protein chemistry and structural biology · doi:10.1016/bs.apcsb.2019.05.002 · Cited by 8
Loss of 5-Hydroxymethylcytosine as an Epigenetic Signature That Correlates With Poor Outcomes in Patients With Medulloblastoma
Zhao, F. Q., Zhang, Z., Zhang, J., Zhang, S., Zhang, H., Zhao, C., Chen, Y., Luo, L., Tong, W., Li, C., et al. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.603686 · Cited by 8
“The TET family consists of three members—TET1, TET2, and TET3—which are responsible for the conversion of 5mC into 5hmC through Fe and a-ketoglutarate-dependent dioxygenase activity (20).”
Background
A non-catalytic role of TET3 promotes open chromatin and enhances global transcriptionPreprint
Krueger, C., Peat, J. R., Eckersley-Maslin, M. A., Hore, T. A., Mohammed, H., Andrews, S., Dean, W., & Reik, W. (2017) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/177626 · Cited by 9
“Dilution or removal of these modified bases is one mechanism by which DNA methylation can be reset in the genome (Branco et al. 2012; Kohli and Zhang 2013; Rasmussen and Helin 2016).”
Background
Glut10 restrains neointima formation by promoting SMCs mtDNA demethylation and improving mitochondrial function
Wu, Q., Hu, Z., Wang, Z., Che, Y., Zhang, M., Zheng, S., Xing, K., Zhong, X., Chen, Y., Shi, F., et al. (2023) · Translational research · doi:10.1016/j.trsl.2023.05.001 · Cited by 7
The role of lncRNAs in the interplay of signaling pathways and epigenetic mechanisms in glioma
Yildiz, C. B., Du, J., Mohan, K. N., Zimmer‐Bensch, G., & Abdolahi, S. (2025) · Epigenomics · doi:10.1080/17501911.2024.2442297 · Cited by 8
Circ_0007919 exerts an anti-tumor role in colorectal cancer through targeting miR-942–5p/TET1 axis
Zhao, X., Cui, D., Fang, Y., Yang, L.-C., & Huang, B. (2021) · Pathology - Research and Practice · doi:10.1016/j.prp.2021.153704 · Cited by 7
Novel prognostic value and potential utility of opioid receptor gene methylation in liquid biopsy for oral cavity cancer
Ishikawa, R., Imai, A., Mima, M., Yamada, S., Takeuchi, K., Mochizuki, D., Shinmura, D., Kita, J., Nakagawa, T., Kurokawa, T., et al. (2022) · Current Problems in Cancer · doi:10.1016/j.currproblcancer.2021.100834 · Cited by 7
Correlation of DNA methylation of DNMT3A and TET2 with oral squamous cell carcinoma
Li, X., Li, Z., Gao, Q., Peng, Y., Yu, Y., Hu, T., & Wang, W. (2024) · Discover Oncology · doi:10.1007/s12672-024-00866-9 · Cited by 7
Epigenetic and gene therapy in human and veterinary medicine
Bártová, E. (2024) · Current Zoology · doi:10.1093/eep/dvae006 · Cited by 11
“Ten-Eleven Translocation (TET1, TET2, and TET3) dioxyge-nases are key players in this epigenetic event [14].”
Background
Glutamine promotes the proliferation of intestinal stem cells via inhibition of TP53-induced glycolysis and apoptosis regulator promoter methylation in burned mice
Zhang, P., Wu, D., Zha, X., Su, S., Zhang, Y., Yan, W., Xia, L., Fan, S., & Peng, X. (2024) · Burns & Trauma · doi:10.1093/burnst/tkae045 · Cited by 9
“Eventually, 5-carboxylcytosine is selectively recognized by thymine-DNA glycosylase and is reversed to unmodified cytosine by base resection repair [33].”
Background
Novel Epigenetics Control (EpC) Nanocarrier for Cancer Therapy Through Dual-Targeting Approach to DNA Methyltransferase and Ten-Eleven Translocation Enzymes
Mitsuhashi, R., Sato, K., & Kawakami, H. (2025) · Epigenomes · doi:10.3390/epigenomes9010006 · Cited by 8
“However, TET mutations are uncommon in solid tumors and are frequently missense mutations that would not significantly impact TET activity [13].”
Prognostic implications of DNA methylation machinery (DNMTs and TETs) expression in gliomas: correlations with tumor grading and patient survival
Sufiyan, S., Salam, H., Ilyas, S., Amin, W., Arshad, F., Fatima, K., Naeem, S., Laghari, A. A., Enam, S. A., & Mughal, N. (2025) · Journal of Neuro-Oncology · doi:10.1007/s11060-025-05032-x · Cited by 7
“Similarly, TET enzymes play dual roles in cancer: Mutations in TET genes, particularly TET2, have been reported in various malignancies including hematologic, renal, prostate, breast, and colorectal [5, 10, 11 ].”
The Epigenetic Progenitor Origin of Cancer Reassessed: DNA Methylation Brings Balance to the Stem Force
Bruschi, M. (2020) · Epigenomes · doi:10.3390/epigenomes4020008 · Cited by 7
“It is currently accepted that the erasure of DNA methylation is not merely due to passive replication-dependent dilution of this mark upon successive cell divisions, but is at least in part mediated by the successive enzymatic oxidation of methylcytosine, catalyzed by the ten-eleven translocation proteins TET1, TET2 a…”
Background
MYC and TFEB Control DNA Methylation and Differentiation in AML
Wu, X., & Eisenman, R. N. (2021) · Blood Cancer Discovery · doi:10.1158/2643-3230.bcd-20-0230 · Cited by 7
Anti-neoplastic and demethylating activity of a newly synthetized flavanone-derived compound in Renal Cell Carcinoma cell lines
Marques-Magalhães, Â., Graça, I. C. R., Miranda‐Gonçalves, V., Henrique, R., Lopez, M., Arimondo, P. B., & Jerónimo, C. (2021) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2021.111681 · Cited by 7
Threshold photoelectron spectroscopy of 9-methyladenine: theory and experiment
Laamiri, K., García, G. A., Nahon, L., Houria, A. B., Feifel, R., & Hochlaf, M. (2021) · Physical Chemistry Chemical Physics · doi:10.1039/d1cp03729c · Cited by 7
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Kalushkova, A., Nylund, P., Párraga, A. A., Lennartsson, A., & Jernberg‐Wiklund, H. (2021) · Epigenomes · doi:10.3390/epigenomes5040022 · Cited by 7
“Additionally, 5hmC itself has roles in modulating chromatin accessibility [11] and enhancer regulation [7,12,13].”
Background
Oncometabolites as Regulators of DNA Damage Response and Repair
Gueble, S. E., & Bindra, R. S. (2021) · Seminars in Radiation Oncology · doi:10.1016/j.semradonc.2021.09.004 · Cited by 8
Targeted demethylation of the SLC5A7 promotor inhibits colorectal cancer progression
Li, Y., Liu, B., Yin, X., Jiang, Z., Fang, C., Chen, N., Zhang, B., Dai, L., & Yin, Y. (2022) · Clinical Epigenetics · doi:10.1186/s13148-022-01308-5 · Cited by 9
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BMP7‐induced osteoblast differentiation requires hedgehog signaling and involves nuclear mechanisms of gene expression control
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“Exceptions to the widespread genomic methylation can be found in gene regulatory regions, such as CpG ‐ rich promoter elements (known as CpG islands), and active enhancers, often associated with a low DNA methylation profile (Rasmussen & Helin, 2016).”
Background
Regional tumour glutamine supply affects chromatin and cell identity
Højfeldt, J. W., & Helin, K. (2016) · Nature Cell Biology · doi:10.1038/ncb3414 · Cited by 7
Self-citation
5-Azacytidine Transiently Restores Dysregulated Erythroid Differentiation Gene Expression in TET2-Deficient Erythroleukemia Cells
Reilly, B. M., Luger, T., Park, S., Lio, C. J., González‐Avalos, E., Wheeler, E. C., Lee, M., Williamson, L. M., Tanaka, T. N., Diep, D. H., et al. (2020) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-20-0453 · Cited by 7
Epigenetic upregulation of TET2 is an independent poor prognostic factor for intrahepatic cholangiocarcinoma
Yamashita, H., Tourna, A., Akita, M., Itoh, T., Chokshi, S., Ajiki, T., Fukumoto, T., Youngson, N. A., & Zen, Y. (2021) · Archiv für Pathologische Anatomie und Physiologie und für Klinische Medicin · doi:10.1007/s00428-021-03251-x · Cited by 7
“Prior to the initiation of the present study, we hypothesised that TET2 may be down-regulated in iCCA, particularly small-duct type cases with wild-type IDH1, similar to haematolymphoid malignancies and diffuse glioma [25].”
Background
RhoC in association with TET2/WDR5 regulates cancer stem cells by epigenetically modifying the expression of pluripotency genes
Thomas, P., Srivastava, S., Udayashankara, A. H., Damodaran, S., Yadav, L., Mathew, B., Suresh, S. B., Mandal, A. K., & Srikantia, N. (2022) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-022-04645-z · Cited by 7
Combination Therapy Approaches to Enhance the Efficacy of ERV-Targeting Vaccines in Cancer
Gracia-Hernandez, M., Maldonado, M. D. M., Schlom, J., & Hamilton, D. H. (2025) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-24-1192 · Cited by 6
“…also found that colorectal and pancreatic tumors that had a viral mimicry phenotype had increased expression of TET2 , a DNA demethylation gene (67), thus suggesting that aberrations in DNA methylation may play an important role in the expression of ERV sequences and in gene signatures of…”
Advances in supplementation strategies for enhancing bovine in vitro embryo production: a review of growth factors and antioxidants
Kereilwe, O. (2025) · Journal of Assisted Reproduction and Genetics · doi:10.1007/s10815-025-03636-w · Cited by 7
“…vitamin C serves as a cofactor for key epigenetic enzymes, including TET methylcytosine dioxygenases and Jumonji C histone demethylases, which regulate DNA and histone demethylation essential for pluri-potency genes (Oct4, Sox2, Cdx2, and Nanog), cell fate, and reprogramming [70, 71, 121–123].”
TET enzymes: Involvement in cancer development and therapeutical perspectives
Aanniz, T., Fessikh, M. E., Touhtouh, J., Aboulaghras, S., Omari, N. E., Khalid, A., Abdalla, A. N., Amanullah, M. R., Goh, B. H., Lee, L., et al. (2025) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2025.195118 · Cited by 7
Decoding the epigenetic landscape: ctDNA methylation as a game-changer in hepatocellular carcinoma management
Yang, D., Yao, Y., Gui, F., Mei, W., & Zeng, C. (2025) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2025.189497 · Cited by 6
The TET/5hmC mediated epigenetic landscape in glioma: From molecular mechanisms to therapeutic targeting and future perspectives
He, J., Peng, F., Xu, Y., Liu, Z., Su, K., Zhou, Y., Jiang, Y., & Wang, M. (2026) · Pharmacological Research · doi:10.1016/j.phrs.2026.108095 · Cited by 8
Epigenetic consequences of DNA damage
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Oxidative Stress and DNA Epigenetic Modifications in Cancer: Mechanisms and Targeted Therapeutics
Yang, X., Chen, Q., Yu, Y., Zang, Y., Zheng, R., Zhang, Z., Lu, S., & Zhou, L. (2026) · MedComm – Oncology · doi:10.1002/mog2.70065 · Cited by 7
DNA methylation in the genesis, progress and prognosis of head and neck cancer
Guo, Z., Liu, W., Yang, Y., Zhang, S., Li, C., & Yang, W. (2023) · Holistic Integrative Oncology · doi:10.1007/s44178-023-00037-w · Cited by 6
“These products were regarded as intermediates in the process from 5mC to unmethylated cytosines [98].”
Background
FH-mutant glioma displaying the epigenetic signature of IDH-mutant astrocytomas
Zschernack, V., Thomas, C., Schaub, C., Kristiansen, G., Waha, A., Goschzik, T., Herrlinger, U., & Pietsch, T. (2024) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlae064 · Cited by 5
Interplay between pioneer transcription factors and epigenetic modifiers in cell reprogramming
Mirizio, G. G., Sampson, S., & Iwafuchi, M. (2024) · Regenerative Therapy · doi:10.1016/j.reth.2024.12.014 · Cited by 6
“Demethylation can occur passively through DNA replication or actively via enzymatic oxidization of the methyl group [64,65].”
Epigenetic control of cell identities from epiblast to gastrulation
Schüle, K. M., & Probst, S. (2025) · FEBS Journal · doi:10.1111/febs.70024 · Cited by 8
“Of the three Tet enzymes, Tet1 and Tet2 , are highly expressed in the pluripotent cells of the ICM (reviewed by [100]) where Tet1 expression is maintained until E6.”
Portable, Wireless Potentiostat Sensor for Ultra-Sensitive, Real-Time Detection of 5hmC in Genomic DNA Using Tree-Like Graphene
Imran, H., Lim, S.-M., Alam, A., An, J., Ko, M., & Lim, S. (2025) · ACS Nano · doi:10.1021/acsnano.4c18646 · Cited by 6
Genetic hypothesis for the developmental origins of health and disease theory
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TET1 Interacts Directly with NANOG via Independent Domains Containing Hydrophobic and Aromatic Residues
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“Demethylation of DNA is mediated by the ten-eleven translocation (TET) protein family (TET1/2/3), which converts 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC) during DNA demethylation [170].”
Induction of cytotoxic effects and changes in DNA methylation-related gene expression in a human fibroblast cell line by the metal–organic framework [H2NMe2]3 [Tb(III)(2,6 pyridinedicarboxylate)3] (Tb-MOF)
Carrillo‐Cocom, L. M., Juárez-Méndez, L., Rincón, S., Rivera, J. M., Nic-Can, G. I., & Zepeda, A. (2023) · Environmental Science and Pollution Research · doi:10.1007/s11356-023-25314-z · Cited by 6
“…translocation enzymes (TET1, TET2, and TET3) through 5-mC oxidation to hydroxymethylcytosine (5-hmC) and further oxidation products, which play an essential role in proper gene regulation, cell differentiation, genome integrity, and several biological processes (Rasmussen and Helin 2016).”
BackgroundInfluential
Cooperation between NSPc1 and DNA methylation represses HOXA11 expression and promotes apoptosis of trophoblast cells during preeclampsia
Xie, L., Ding, N., Sheng, S., Zhang, H., Yin, H., Gao, L., Zhang, H., Ma, S., Yang, A., Li, G., et al. (2023) · Acta Biochimica et Biophysica Sinica · doi:10.3724/abbs.2023012 · Cited by 6
“The ten eleven translocation (TET) enzymes oxidize 5mC and promote locus-specific reversal of DNA methylation to activate DNA demethylation [39].”
A Thermodynamic Approach to the Metaboloepigenetics of Cancer
Lucia, U., Deisboeck, T. S., Ponzetto, A., & Grisolia, G. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24043337 · Cited by 6
“TET genes are frequently mutated in various cancers, and they play an important role in tumorigenesis due to their role in regulating DNA methylation and transcription [22]; indeed, cancer initiation and progression are related to modifications of DNA methylation [23].”
Background
The Tet2–Upf1 complex modulates mRNA stability under stress conditions
Xia, M., Yan, R., Wang, W., Kong, A., Zhang, M., Miao, Z., Ge, W., Wan, B., & Xu, X. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2023.1158954 · Cited by 6
“(E–G) Quantitative RT-PCR of Tet1 (E), Tet2 (F), and Tet3 (G)mRNA levels in the hippocampus of control and CMS mice. n = 3, *p < 0.05, **p < 0.01.”
BackgroundInfluential
The role of epigenetic changes in the pathology and treatment of inherited retinal diseases
Miller, A. L., James, R. E., Harvey, A. R., Trifunović, D., & Carvalho, L. S. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1224078 · Cited by 6
“The level of methylation and demethylation of DNA is modulated by DNA methyltransferases (DNMTs) and ten-eleven translocase (TET) enzymes (Figure 1) (Moore et al., 2013; Rasmussen and Helin, 2016).”
Background
Association between SPRY1 and TET3 in skin photoaging and natural aging mechanisms
Qiu, B., Yang, E., Zheng, Y., & Hengshu, Z. (2023) · Journal of Cosmetic Dermatology · doi:10.1111/jocd.16115 · Cited by 6
TNC upregulation promotes glioma tumourigenesis through TDG-mediated active DNA demethylation
Xu, H., Long, S., Xu, C., Li, Z., Chen, J., Yang, B., He, Y., Xu, Z., Li, Z., Wei, W., et al. (2024) · Cell Death Discovery · doi:10.1038/s41420-024-02098-w · Cited by 6
“Although most research has focused on the ten eleven translocation (TET) family, studies on thymine DNA glycosylase (TDG) are relatively limited [17, 18].”
Background
The effects of TETs on DNA methylation and hydroxymethylation of mouse oocytes after vitrification and warming
Fu, L., Chang, H., Wang, Z., Xie, X., Chen, H., lei, Z., Zhang, Y., & Quan, F. (2019) · Cryobiology · doi:10.1016/j.cryobiol.2019.09.001 · Cited by 6
SERS-Based Assessment of MRD in Acute Promyelocytic Leukemia?
Turcas, C., Moisoiu, V., Ştefancu, A., Jurj, A. M., Iancu, Ș. D., Teodorescu, P., Paşca, S., Bojan, A. S., Trifa, A. P., Iluta, S., et al. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.01024 · Cited by 6
“The opposing mechanism to DNA methylation, DNA demethylation, can take place actively, via the action of Teneleven translocation (TET) methyl cytosine dioxygenases, which progressively oxidize 5-mC to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5-fC), and 5-carboxylcytosine (5-caC) (10).”
Background

Authors: Rasmussen, K. D., & Helin, K.
Affiliations: University of Copenhagen (DK)
Corresponding author: Helin, Kristian
ORCID: Rasmussen, Kasper Dindler
Helin, Kristian
Venue: Genes & Development
Publisher: Cold Spring Harbor Laboratory
Published: 2016-04-01
Volume: 30
Issue: 7
Pages: 733-750
ISSN: 0890-9369 (ISSN-L)
1549-5477
DOI: 10.1101/gad.276568.115
PMC: PMC4826392
OpenAlex: W2325267338
Cited by: 1,040
References: 162
Citations by year: 2026: 56 · 2025: 87 · 2024: 116 · 2023: 100 · 2022: 135 · 2021: 141 · 2020: 131 · 2019: 97 · 2018: 83 · 2017: 60 · 2016: 30
Type: posted content
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc
Locations: Genes & Development (publishedVersion, cc-by-nc)
PubMed Central (publishedVersion, cc-by-nc)
PubMed (publishedVersion)
Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by-nc)
HighWire Press Open Archive (submittedVersion)
Funders: Danish Medical Research Council (1333-00120B)
European Research Council (294666_DNAMET)
Danish Cancer Society
Danish National Research Foundation (DNRF 82)
Danish Council for Strategic Research
Novo Nordisk Foundation
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer-related gene regulation
Keywords: TET enzymes, DNA methylation, 5-methylcytosine oxidation, TET2, demethylation, cancer, developmental regulation, transcriptional regulation, gene expression
MeSH terms: Animals, Cytosine, DNA-Binding Proteins, Humans, Neoplasms, Oxidation-Reduction, Proto-Oncogene Proteins, Gene Expression Regulation, Neoplastic, DNA Methylation, Epigenesis, Genetic, Dioxygenases

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Role of TET enzymes in DNA methylation, development, and cancer

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