ArticleCell reports2014
Suppression of TET1-dependent DNA demethylation is essential for KRAS-mediated transformation.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 69 citations in OpenAlex.
- Oncogenic RAS as an adaptive signaling ecosystem: context-dependent vulnerabilities and resistance-informed therapeutic design.Experimental hematology & oncology · 2026Review
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- Heat-Stressed Brains: Epigenetic and Mitochondrial Signatures in Zebrafish.Molecular neurobiology · 2025Article
- Elucidating Ras protein as a dual therapeutic target for inflammation and cancer: a review.Discover oncology · 2025Review
- System genetic analysis of intestinal cancer and periodontitis development as influenced by aging and diabesity using Collaborative Cross mice.Animal models and experimental medicine · 2025Review
- A narrative review of epigenetic marker in H3K27ac and its emerging potential as a therapeutic target in cancer.Epigenomics · 2025Review
- SilencingEnvironmental epigenetics · 2025Article
- ZBTB20 suppresses tumor growth in glioblastoma through activating the TET1/FAS/caspase‑3 pathway.Oncology letters · 2024Article
- Tumor hypoxia: From basic knowledge to therapeutic implications.Seminars in cancer biology · 2023Review
- Regulation of paternal 5mC oxidation and H3K9me2 asymmetry by ERK1/2 in mouse zygotes.Cell & bioscience · 2022Article
- Article
- Integration of Epigenetic Mechanisms into Non-Genotoxic Carcinogenicity Hazard Assessment: Focus on DNA Methylation and Histone Modifications.International journal of molecular sciences · 2021Review
- D-2-Hydroxyglutarate in Glioma Biology.Cells · 2021Review
- Ten-eleven translocase: key regulator of the methylation landscape in cancer.Journal of cancer research and clinical oncology · 2021Review
- Ten-Eleven Translocation 1 Promotes Malignant Progression of Cholangiocarcinoma With Wild-Type Isocitrate Dehydrogenase 1.Hepatology (Baltimore, Md.) · 2021Article
- Oncolytic Virotherapy: The Cancer Cell Side.Cancers · 2021Review
- Deoxyribonucleic Acid 5-Hydroxymethylation in Cell-Free Deoxyribonucleic Acid, a Novel Cancer Biomarker in the Era of Precision Medicine.Frontiers in cell and developmental biology · 2021Review
- Ochratoxin A-induced genotoxic and epigenetic mechanisms lead to Alzheimer disease: its modulation with strategies.Environmental science and pollution research international · 2020Review
- 2-Oxoglutarate-dependent dioxygenases in cancer.Nature reviews. Cancer · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Hypermethylation-mediated tumor suppressor gene (TSG) silencing is a central epigenetic alteration in RAS-dependent tumorigenesis. Ten-eleven translocation (TET) enzymes can depress DNA methylation by hydroxylation of 5-methylcytosine (5mC) bases to 5-hydroxymethylcytosine (5hmC). Here, we report that suppression of TET1 is required for KRAS-induced DNA hypermethylation and cellular transformation. In distinct nonmalignant cell lines, oncogenic KRAS promotes transformation by inhibiting TET1 expression via the ERK-signaling pathway. This reduces chromatin occupancy of TET1 at TSG promoters, lowers levels of 5hmC, and increases levels of 5mC and 5mC-dependent transcriptional silencing. Restoration of TET1 expression by ERK pathway inhibition or ectopic TET1 reintroduction in KRAS-transformed cells reactivates TSGs and inhibits colony formation. KRAS knockdown increases TET1 expression and diminishes colony-forming ability, whereas KRAS/TET1 double knockdown bypasses the KRAS dependence of KRAS-addicted cancer cells. Thus, suppression of TET1-dependent DNA demethylation is critical for KRAS-mediated transformation.
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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.