ArticleOncology letters2017
Epigallocatechin-3-gallate inhibits growth and induces apoptosis in esophageal cancer cells through the demethylation and reactivation of the p16 gene.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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.
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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
9 citing papers in PubMed.
- Green Tea (Foods (Basel, Switzerland) · 2021Article
- The Impact of EGCG and RG108 on SOCS1 Promoter DNA Methylation and Expression in U937 Leukemia Cells.Reports of biochemistry & molecular biology · 2021Article
- Carboplatin and epigallocatechin-3-gallate synergistically induce cytotoxic effects in esophageal cancer cells.Research in pharmaceutical sciences · 2021Article
- Identification of serum prognostic marker miRNAs and construction of microRNA-mRNA networks of esophageal cancer.PloS one · 2021Article
- The Impact of Natural Dietary Compounds and Food-Borne Mycotoxins on DNA Methylation and Cancer.Cells · 2020Review
- Telomerase Biology Associations Offer Keys to Cancer and Aging Therapeutics.Current aging science · 2020Review
- Advances in the Antagonism of Epigallocatechin-3-gallate in the Treatment of Digestive Tract Tumors.Molecules (Basel, Switzerland) · 2019Review
- Inhibitory Effects of (-)-Epigallocatechin-3-gallate on Esophageal Cancer.Molecules (Basel, Switzerland) · 2019Review
- Dietary Compounds as Epigenetic Modulating Agents in Cancer.Frontiers in genetics · 2019Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the effect of treatment with epigallocatechin-3-gallate (EGCG) on the human esophageal cancer cell line ECa109 and elucidate the associated underlying mechanisms. ECa109 cells were cultured and treated with increasing concentrations of EGCG for various durations. Cell viability was evaluated using the MTT assay and apoptosis was detected using flow cytometry. The methylation status of the cyclin-dependent kinase inhibitor 2A (p16) gene was analyzed using the methylation-specific polymerase chain reaction (PCR). p16 mRNA and protein expression was measured using reverse transcription-quantitative PCR and western blot analysis, respectively. The results of the present study demonstrated that, following treatment with EGCG, ECa109 cell viability was significantly decreased, while the rate of apoptosis was significantly increased (P<0.01), in a dose- and time-dependent manner. Following treatment of ECa109 cells with EGCG, p16 gene demethylation, and its mRNA and protein expression, were significantly increased compared with the untreated cells (P<0.01). EGCG may induce ECa109 cell apoptosis and inhibit cell growth through p16 gene demethylation, which restores its expression.
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Registered trials
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