ArticleCancer science2018
Aberrant methylation of EYA4 promotes epithelial-mesenchymal transition in esophageal squamous cell carcinoma.
Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma and its Clinical Implications in Systemic Chemotherapy.International journal of medical sciences · 2025Review
- Exploring Potential Biomarkers in Oesophageal Cancer: A Comprehensive Analysis.International journal of molecular sciences · 2024Review
- Cellular and clinical impact of protein phosphatase enzyme epigenetic silencing in multiple cancer tissues.Human genomics · 2024Article
- Targeting epigenetic deregulations for the management of esophageal carcinoma: recent advances and emerging approaches.Cell biology and toxicology · 2023Review
- EYA4 promotes breast cancer progression and metastasis through its role in replication stress avoidance.Molecular cancer · 2023Article
- EYA4 drives breast cancer progression and metastasis through its novel role in replication stress avoidance.Research square · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Tripartite motif containing 69 elicits ERK2-dependent EYA4 turnover to impart pancreatic tumorigenesis.Journal of Cancer · 2023Article
- CXCR4 promotes the growth and metastasis of esophageal squamous cell carcinoma as a critical downstream mediator of HIF-1α.Cancer science · 2022Article
- Cigarette Smoke Regulates the Expression of EYA4 via Alternation of DNA Methylation Status.BioMed research international · 2022Article
- Epigenetic modifications in esophageal cancer: An evolving biomarker.Frontiers in genetics · 2022Review
- Novel Methylation Biomarkers for Colorectal Cancer Prognosis.Biomolecules · 2021Review
- Subclone Eradication Analysis Identifies Targets for Enhanced Cancer Therapy and Reveals L1 Retrotransposition as a Dynamic Source of Cancer Heterogeneity.Cancer research · 2021Article
- Aberrant DNA Methylation in Esophageal Squamous Cell Carcinoma: Biological and Clinical Implications.Frontiers in oncology · 2020Review
- EYA4 inhibits hepatocellular carcinoma by repressing MYCBP by dephosphorylating β-catenin at Ser552.Cancer science · 2019Article
- The clinical significance of HOXA9 promoter hypermethylation in head and neck squamous cell carcinoma.Journal of clinical laboratory analysis · 2019Article
- Circular RNA ACVR2A suppresses bladder cancer cells proliferation and metastasis through miR-626/EYA4 axis.Molecular cancer · 2019Article
- Epigenetics mechanisms mediate the miR-125a/BRMS1 axis to regulate invasion and metastasis in gastric cancer.OncoTargets and therapy · 2019Article
- Aberrant methylation of EYA4 promotes epithelial-mesenchymal transition in esophageal squamous cell carcinoma.Cancer science · 2018Article
- Aberrant DNA methylation and expression ofSaudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationArticle
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EYA4, one of the four members of the EYA gene family, is associated with several human cancers. However, its biological functions and molecular mechanisms in the progression of cancer, particularly in esophageal squamous cell carcinoma (ESCC), remain unknown. In the present study, we found that EYA4 was underexpressed and hypermethylated in most of the ESCC cell lines tested (85.7%, 6/7). Treatment with 5-aza-dC and/or trichostatin A (TSA) restored EYA4 expression in ESCC cell lines, which indicates that EYA4 expression was epigenetically regulated. Similarly, EYA4 was aberrantly hypermethylated in ESCC tissues (78%, 39/50) and downregulation of EYA4 occurred in approximately 65% of primary ESCC at protein level where it was associated significantly with TNM stage and lymph node metastases. Knockdown of EYA4 in KYSE30 and KYSE70 ESCC cells using small hairpin RNA increased migration and invasive motility in vitro. Conversely, the overexpression of EYA4 in KYSE180 and KYSE450 promoted an epithelial phenotype, which consisted of decreased migration and invasion abilities and a decrease in TGF-β1-induced epithelial-mesenchymal transition. Mechanistically, EYA4 overexpression reduced the phosphorylation of Akt and glycogen synthase kinase (GSK) 3β, which led to the inactivation of slug. In addition, we found that TGF-β1 decreased EYA4 expression in both a dose-dependent and a time-dependent manner in KYSE30 cells, accompanied by an increase in the expression of DNA methyltransferases, especially DNMT3A. In summary, EYA4 is frequently hypermethylated in ESCC and may function as a tumor suppressor gene in the development of ESCC.
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