ArticleProceedings of the National Academy of Sciences of the United States of America1995
Silencing of the E-cadherin invasion-suppressor gene by CpG methylation in human carcinomas.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 4 of them syntheses 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.
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Who cites it
212 citing papers in PubMed, 4 syntheses or guidelines pooled it, 665 citations in OpenAlex.
- Pooled it
- The association between CDH1 promoter methylation and patients with ovarian cancer: a systematic meta-analysis.Journal of ovarian research · 2016Pooled it
- E-cadherin gene methylation in lung cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- [Meta-analysis of association between E-cadherin promoter methylation and lung cancer risk].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2013Pooled it
- Whole-genome methylation sequencing reveals distinct impact of differential methylations on gene transcription in prostate cancer.The American journal of pathology · 2013Trial
- Trial
- DNA methyltransferase inhibitors in oncology: clinical progress, limitations and future directions.Epigenomics · 2026Review
- Insight into the role of DNA methylation in prognosis and treatment response prediction of gastrointestinal cancers.Epigenomics · 2025Review
- NSD3 protein methylation and stabilization transforms human ES cells into variant state.Life science alliance · 2025Article
- A subset of Polycomb-targeted transcription factor genes become hypermethylated yet upregulated in colorectal cancer.Computational and structural biotechnology journal · 2025Article
- Molecular pathological approach to cancer epigenomics and its clinical application.Pathology international · 2024Review
- Epigenetic Alteration in Colorectal Cancer: Potential Diagnostic and Prognostic Implications.International journal of molecular sciences · 2024Review
- Dynamic interplay of nuclear receptors in tumor cell plasticity and drug resistance: Shifting gears in malignant transformations and applications in cancer therapeutics.Cancer metastasis reviews · 2024Review
- Crosstalk between metabolic reprogramming and epigenetics in cancer: updates on mechanisms and therapeutic opportunities.Cancer communications (London, England) · 2022Review
- A functional SNP regulates E-cadherin expression by dynamically remodeling the 3D structure of a promoter-associated non-coding RNA transcript.Nucleic acids research · 2022Article
- Review
- Loss of E-cadherin Induces IGF1R Activation and Reveals a Targetable Pathway in Invasive Lobular Breast Carcinoma.Molecular cancer research : MCR · 2022Article
- Promoter hypermethylation of GALR1 acts as an early epigenetic susceptibility event in colorectal carcinogenesis.Journal of human genetics · 2022Article
- Bioinformatics analysis and identification of genes and pathways involved in patients with Wilms tumor.Translational cancer research · 2022Article
- Identification of EMT-Related Genes and Prognostic Signature With Significant Implications on Biological Properties and Oncology Treatment of Lower Grade Gliomas.Frontiers in cell and developmental biology · 2022Article
152 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
E-Cadherin, a cell adhesion molecule, which plays a key role in maintaining the epithelial phenotype, is regarded as an invasion-suppressor gene in light of accumulating evidence from in vitro experiments and clinical observations. In an attempt to clarify the mechanism responsible for inactivation of this gene in carcinomas, we investigated the methylation state around the promoter region by digestion of DNA with the methylation-sensitive restriction enzyme Hpa II, as CpG methylation of the promoter has been postulated to be a mechanism of transcriptional inactivation of some genes. We found that E-cadherin expression-negative carcinoma cell lines were accompanied by the hypermethylation state, whereas E-cadherin-positive cell lines were not. Furthermore, treatment of E-cadherin-negative carcinoma cells with the demethylating agent 5-azacytidine resulted in reexpression of the gene and reversion of scattered spindle-shaped cells to cells with epithelial morphology. These results suggest that hypermethylation around the promoter may be a mechanism of E-cadherin inactivation in human carcinomas and that treatment of E-cadherin-inactivated cells with a demethylating agent may cause gene expression reversion leading to epithelial morphogenesis with acquisition of the homophilic cell-cell adhesive property.
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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.