ArticleCell death & disease2017
MicroRNA-29a induces loss of 5-hydroxymethylcytosine and promotes metastasis of hepatocellular carcinoma through a TET-SOCS1-MMP9 signaling axis.
Article in Cell death & disease, 2017. 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 54 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Prognostic role of high TET1 expression in patients with solid tumors: A meta-analysis.Medicine · 2020Pooled it
- Detection of miR‑29a in plasma of patients with lumbar spinal stenosis and the clinical significance.Molecular medicine reports · 2018Trial
- Epitranscriptomic control of cancer: the emerging roles of m⁵C and ac⁴C RNA modifications.Cell death discovery · 2026Review
- A demethylation-driven gene signature predicts prognosis and therapeutic vulnerability in hepatocellular carcinoma.Scientific reports · 2026Article
- 5-mC RNA methylation: a key regulator in cancer development and treatment.Journal of translational medicine · 2026Review
- Article
- Rewriting the Fate of Cancer: Epigenetic and Epitranscriptomic Regulators in the Metastatic Cascade.Biomolecules · 2025Review
- TRIM8 Promotes Proliferation, Invasion, and Migration of Cervical Cancer Cells by Ubiquitinating and Degrading SOCS1.Biochemical genetics · 2025Article
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- The epigenetic basis of hepatocellular carcinoma - mechanisms and potential directions for biomarkers and therapeutics.British journal of cancer · 2025Review
- FTO downregulation-mediated m6A modification resulting in enhanced hepatocellular carcinoma invasion.Cell & bioscience · 2025Article
- The secrets of menstrual blood: emerging frontiers from diagnostic tools to stem cell therapies.Frontiers in cell and developmental biology · 2025Review
- The role of TET2 in solid tumors and its therapeutic potential: a comprehensive review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- ncRNAs-mediated overexpression ofHeliyon · 2024Article
- Emerging role of MicroRNA-Based theranostics in Hepatocellular Carcinoma.Molecular biology reports · 2023Review
- Associations Between Epigenetic Age Acceleration and microRNA Expression Among U.S. Firefighters.Epigenetics insights · 2023Article
- DNA methylation in cell plasticity and malignant transformation in liver diseases.Pharmacology & therapeutics · 2023Review
- Mechanisms that regulate the activities of TET proteins.Cellular and molecular life sciences : CMLS · 2022Review
- Epigenetic Regulation in Uterine Fibroids-The Role of Ten-Eleven Translocation Enzymes and Their Potential Therapeutic Application.International journal of molecular sciences · 2022Review
- Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ten eleven translocation (TET) enzymes convert 5-methylcytosine (5-mC) to 5-hydroxy-methylcytosine (5-hmC) and have crucial roles in biological and pathological processes by mediating DNA demethylation, however, the functional role of this epigenetic mark and the related enzymes in hepatocellular carcinoma (HCC) progression remains unknown. Here, we demonstrated that TET-family enzymes downregulation was one likely mechanism underlying 5-hmC loss in HCC. We found that miR-29a overexpression increased DNA methylation of suppressor of cytokine signaling 1 (SOCS1) promoter was associated with HCC metastasis in vitro and in vivo. Furthermore, miR-29a silenced anti-metastatic SOCS1 through direct TET-family targeting, resulting in SOCS1 promoter demethylation inhibition. Chromatin immunoprecipitation analyses confirmed that TET1 regulated SOCS1 expression through binding to the promoter region of SOCS1. Finally, miR-29a overexpression correlated with poor clinical outcomes and TET-SOCS1-matrix metalloproteinase (MMP) 9 axis silencing in HCC patients. In conclusion, our findings demonstrate that 5-hmC loss is an epigenetic hallmark of HCC, and miR-29a is an important epigenetic modifier, promoting HCC metastasis through TET-SOCS1-MMP9 axis silencing. The results offer a new strategy for epigenetic cancer therapy.
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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.