ArticleOncotarget2017
Epigenetic silencing of TET2 and TET3 induces an EMT-like process in melanoma.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 62 citations in OpenAlex.
- Increasing TET Expression and 5-Hydroxymethylcytosine Formation by a Carbocyclic 5-Aza-2'-deoxy-cytidine Antimetabolite.Angewandte Chemie (International ed. in English) · 2026Article
- 5-Hydroxymethylcytosine: a key epigenetic mark in cancer and chemotherapy response.Epigenetics & chromatin · 2025Review
- DNA-methylation eraser TET2 activates WTIP expression to suppress an AKT-dependent chemoresistance of gastric cancer.Neoplasia (New York, N.Y.) · 2025Article
- Epigenetic Therapies in Melanoma-Targeting DNA Methylation and Histone Modification.Biomedicines · 2025Review
- Loss of tet methyl cytosine dioxygenase 3 (TET3) enhances cardiac fibrosis via modulating the DNA damage repair response.Clinical epigenetics · 2024Article
- Downregulation of TET2 Contributes to Nasal Polypogenesis Through Hypoxia-Inducible Factor 1α-Mediated Epithelial-to-Mesenchymal Transition.Clinical and experimental otorhinolaryngology · 2024Article
- Correlation of DNA methylation of DNMT3A and TET2 with oral squamous cell carcinoma.Discover oncology · 2024Article
- Cancer metastasis under the magnifying glass of epigenetics and epitranscriptomics.Cancer metastasis reviews · 2023Review
- Standardized Computer-Assisted Analysis of 5-hmC Immunoreactivity in Dysplastic Nevi and Superficial Spreading Melanomas.International journal of molecular sciences · 2023Article
- The novel oncogenic factor TET3 combines with AHR to promote thyroid cancer lymphangiogenesis via the HIF-1α/VEGF signaling pathway.Cancer cell international · 2023Article
- Review
- Epigenetic Regulators of DNA Cytosine Modification: Promising Targets for Cancer Therapy.Biomedicines · 2023Review
- Characterization of the CpG Island Hypermethylated Phenotype Subclass in Primary Melanomas.The Journal of investigative dermatology · 2022Article
- Distinct cytosine modification profiles define epithelial-to-mesenchymal cell-state transitions.Epigenomics · 2022Article
- Differential Expression of Steroid Hormone Receptors and Ten Eleven Translocation Proteins in Endometrial Cancer Cells.Frontiers in oncology · 2022Article
- Cancer Cell Phenotype Plasticity as a Driver of Immune Escape in Melanoma.Frontiers in immunology · 2022Review
- Ten-eleven translocase: key regulator of the methylation landscape in cancer.Journal of cancer research and clinical oncology · 2021Review
- The Potential Equivalents ofCancers · 2021Review
- Runx3 Induces a Cell Shape Change and Suppresses Migration and Metastasis of Melanoma Cells by Altering a Transcriptional Profile.International journal of molecular sciences · 2021Article
- Restoration of TET2 deficiency inhibits tumor growth in head neck squamous cell carcinoma.Annals of translational medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-Mesenchymal Transition (EMT) is a critical step in the progression of cancer. Malignant melanoma, a cancer developed from pigmented melanocytes, metastasizes through an EMT-like process. Ten-eleven translocation (TET) enzymes, catalyzing the conversion of 5-methylcytosine (5mC) to 5-hydroxylmethylcytosine (5-hmC), are down regulated in melanoma. However, their roles in the progression and the EMT-like process of melanoma are not fully understood. Here we report that DNA methylation induced silencing of TET2 and TET3 are responsible for the EMT-like process and the metastasis of melanoma. TET2 and TET3 are down regulated in the TGF-β1-induced EMT-like process, and the knocking down of TET2 or TET3 induced this EMT-like process. A DNA demethylating agent antagonized the TGF-β-induced suppression of TET2 and TET3. Furthermore, a ChIP analysis indicated that enhanced recruitment of DNMT3A (DNA Methyltransferase 3A) is the mechanism by which TGF-β induces the silencing of TET2 and TET3. Finally, the overexpression of the TET2 C-terminal sequence partially rescues the TGF-β1-induced EMT-like process in vitro and inhibits tumor growth and metastasis in vivo. Hence, our data suggest an epigenetic circuitry that mediates the EMT activated by TGF-β. As an effector, DNMT3A senses the TGF-β signal and silences TET2 and TET3 promoters to induce the EMT-like process and metastasis in melanoma.
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Registered trials
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.