Evidence map›Paper›PMID 31810492›Full record

ArticleClinical epigenetics2019

DNMT1 recruited by EZH2-mediated silencing of miR-484 contributes to the malignancy of cervical cancer cells through MMP14 and HNF1A.

Yang Hu, Fuxia Wu, Yankun Liu, Qian Zhao, Hua Tang

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 92 citations in OpenAlex.

  1. Review
  2. Article
  3. Matrix Metalloproteinase 14 in Corneal Neovascularization.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Missense and Intronic Variants inInternational journal of medical sciences · 2026
    Article
  6. Review
  7. Article
  8. DNMT Enzymes and Their Impact on Cervical Cancer: A State-of-the-Art Review.International journal of molecular sciences · 2025
    Review
  9. Activation of epigenetic reprogramming via crotonylation overcomes resistance to EGFR-TKI therapy in lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  11. Article
  12. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Yang HuTianjin Life Science Research Center, Tianjin Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, Basic Medical School, Tianjin Medical University, 22 Qi-Xiang-Tai Road, Tianjin, 300070, China.
Fuxia WuTianjin Life Science Research Center, Tianjin Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, Basic Medical School, Tianjin Medical University, 22 Qi-Xiang-Tai Road, Tianjin, 300070, China.
Yankun LiuThe Cancer Institute, Tangshan People's Hospital, Tangshan, 063001, China.
Qian ZhaoDepartment of Cell Biology, Tianjin Medical University, Tianjin, 300070, China.
Hua TangTianjin Life Science Research Center, Tianjin Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, Basic Medical School, Tianjin Medical University, 22 Qi-Xiang-Tai Road, Tianjin, 300070, China. htang2002@yahoo.com.
Tianjin Medical University · CNTangshan People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEmerging evidence indicates that dysregulation of microRNAs (miRNAs) contributes to cervical cancer (CC) tumorigenesis and development. Previous work showed that miR-484 which regulated the EMT process was obviously downregulated in CC. However, little is known about the precise mechanism.

resultsWe found that the deficiency of EZH2-recruited DNA methyltransferases DNMT1 reduced the CpG methylation of miR-484 promoter and then increased the miR-484 expression. Furthermore, the cell membrane-bound matrix metalloproteinase (MMP14) and the hepatocyte nuclear factor 1A (HNF1A) were found to be downregulated by miR-484. miR-484 repressed the expression of MMP14 and HNF1A inhibiting CC growth and metastasis in vitro and in vivo. Upregulation of MMP14 and HNF1A promotes the CC cell adhesion and EMT, all of which contribute to cell motility and metastasis. Moreover, miR-484 negatively regulates the WNT/MAPK and TNF signaling pathway by downregulating HNF1A and MMP14 respectively. Thus, miR-484, who is downregulated by DNMT1-mediated hypermethylation in its promoter, functions as a tumor suppressor by inhibiting MMP14 and HNF1A expression in CC.

conclusionOur finding characterizes miR-484 as a key suppressive regulator in CC metastasis and reveals a DNMT1-mediated epigenetic mechanism for miR-484 silencing, expanding our understanding of the molecular mechanism underlying CC progression and metastasis.

Indexed as

Down-RegulationAnimalsCell Line, TumorCell ProliferationDNA (Cytosine-5-)-Methyltransferase 1Enhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHeLa CellsHepatocyte Nuclear Factor 1-alphaHumansMatrix Metalloproteinase 14MiceMicroRNAsDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHepatocyte Nuclear Factor 1-alphaHNF1A protein, humanMatrix Metalloproteinase 14MicroRNAsMIRN484 microRNA, humanMMP14 protein, humanCervical cancerDNA methylationDNMT1Histone modificationmiR-484

Identifiers

PMID31810492
PMCPMC6898970
OpenAlexW2992037378

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.