ArticleCell death & disease2020
Epigenetic silencing of ZIC4 contributes to cancer progression in hepatocellular carcinoma.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Detection of Circulating Cell-free DNA to Diagnose Hepatocellular Carcinoma in Chinese Population: A Systematic Review and Meta-analysis.Current medicinal chemistry · 2024Pooled it
- Integrative multi-cohort analysis of DNA methylation profiles for pancreatic ductal adenocarcinoma biomarker discovery and prognosis.Frontiers in bioinformatics · 2026Article
- The multifaceted roles of ZIC genes in cancer: from development regulators to cancer modulators.Discover oncology · 2025Review
- Serum Onconeural Antibodies in Dogs and Cats for Early Diagnosis of Cancer.Veterinary medicine (Auckland, N.Z.) · 2025Article
- Homeobox B9 promotes the invasion and metastasis of hepatocellular carcinoma cells via the EZH2-MIR203A-SNAI2 axis.Journal of translational medicine · 2024Article
- Epigenetic silencing of ZIC4 unveils a potential tumor suppressor role in pediatric choroid plexus carcinoma.Scientific reports · 2024Article
- Multi-tissue DNA methylation aging clocks for sea lions, walruses and seals.Communications biology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inactivation of tumor suppressor gene played critical roles in the development and progression of human hepatocellular carcinoma (HCC). Zic family member 4 (ZIC4) is transcription factor and plays an important role in the developmental process. However, the expression and biological role of ZIC4 in HCC is poorly understood. Here, bioinformatics analysis based on The Cancer Genome Atlas (TCGA) database revealed an aberrant hypermethylation of ZIC4 in HCC. ZIC4 is frequently hypermethylated in promoter region and down expressed in HCC cells and tissues. Functionally, ZIC4 inhibition facilitated the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in vitro and in vivo. Conversely, ZIC4 overexpression reduced proliferation and invasiveness of HCC cells. In addition, ZIC4 inhibition rescued the antitumor effect induced by enhancer of zeste homolog 2 (EZH2) knockdown or EZH2 inhibitor. Mechanistically, EZH2 knockdown or EZH2 inhibitor reduced the enrichment of EZH2 and H3K27me3 in ZIC4 promoter region and leading to the upregulation of ZIC4. Altogether, these data indicate that epigenetic silencing of ZIC4 by EZH2 mediated H3K27me3 is an important mechanism in HCC and provide a new therapeutic target for the treatment of hepatocellular carcinoma disease.
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Registered trials
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