ArticleJournal of Cancer2014
Regulation of Desmocollin3 Expression by Promoter Hypermethylation is Associated with Advanced Esophageal Adenocarcinomas.
Article in Journal of Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Evaluating Potential Therapeutic Targets and Drug Repurposing Based on the Esophageal Cancer Subtypes.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Review
- Integrated molecular analysis reveals complex interactions between genomic and epigenomic alterations in esophageal adenocarcinomas.Scientific reports · 2017Article
- Emerging therapeutic targets in esophageal adenocarcinoma.Oncotarget · 2016Review
- A genome-wide search for epigenetically [corrected] regulated genes in zebra finch using MethylCap-seq and RNA-seq.Scientific reports · 2016Article
- PCDH8 is Frequently Inactivated by Promoter Hypermethylation in Liver Cancer: Diagnostic and Clinical Significance.Journal of Cancer · 2016Article
- Identification of immunohistochemical markers for distinguishing lung adenocarcinoma from squamous cell carcinoma.Journal of thoracic disease · 2015Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundDesmocollin3 (DSC3) is a member of the cadherin superfamily of calcium-dependent cell adhesion molecules and plays an important role in tumor invasion and metastasis. In this study, we investigated the epigenetic mechanism that regulates DSC3 expression in esophageal adenocarcinomas (EACs).
methodsExpression of DSC3 was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The promoter DNA methylation level of DSC3 was examined using quantitative bisulfite pyrosequencing.
resultsThe qRT-PCR analysis demonstrated significant down-regulation of the DSC3 mRNA levels in human EAC cell lines and tissue samples (P<.001). In addition, the EAC cell lines and tumor samples have aberrant promoter hypermethylation as compared to normal esophageal samples (P<.001). DSC3 promoter hypermethylation (>10% methylation level) was detected in 97.5% (39/40) of EAC samples whereas none of the normal tissue samples showed hypermethylation (P<.0001). There was a significant inverse correlation between promoter DNA methylation levels and mRNA expression folds for DSC3 (coefficient r=-0.685, P<.0001). Treatment of FLO-1 and SKGT4 EAC cells with 5-Aza-deoxytidine led to a significant reduction in the promoter DNA methylation levels with restoration of the DSC3 expression, suggesting that promoter DNA methylation is a key epigenetic mechanism regulating DSC3 expression. High DSC3 promoter DNA methylation levels were significantly correlated with advanced tumor stage (P<.001) and lymph node metastasis (P<.001).
conclusionTaken together, our results demonstrate that epigenetic silencing of DSC3 is a frequent finding in EAC that is possibly associated with advanced stages.
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