ArticleOncology letters2017
Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis in Ec9706 and Eca109 esophageal carcinoma cells.
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 13 papers.
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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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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Discovery and Characterization of a Distinctive Theaflavin-3-Gallate Isomer fromFoods (Basel, Switzerland) · 2025Article
- The Role of Natural Flavonoids as Telomerase Inhibitors in Suppressing Cancer Growth.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Therapeutic Effects of Green Tea Polyphenol (‒)-Epigallocatechin-3-Gallate (EGCG) in Relation to Molecular Pathways Controlling Inflammation, Oxidative Stress, and Apoptosis.International journal of molecular sciences · 2022Review
- Carboplatin and epigallocatechin-3-gallate synergistically induce cytotoxic effects in esophageal cancer cells.Research in pharmaceutical sciences · 2021Article
- Stilbene Compounds Inhibit Tumor Growth by the Induction of Cellular Senescence and the Inhibition of Telomerase Activity.International journal of molecular sciences · 2019Review
- Ribophorin II promotes cell proliferation, migration, and invasion in esophageal cancer cellsBioscience reports · 2019Article
- 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
- EGCG overcomes gefitinib resistance by inhibiting autophagy and augmenting cell death through targeting ERK phosphorylation in NSCLC.OncoTargets and therapy · 2019Article
- Molecular Targets of Epigallocatechin-Gallate (EGCG): A Special Focus on Signal Transduction and Cancer.Nutrients · 2018Review
- Effect of therapies-mediated modulation of telomere and/or telomerase on cancer cells radiosensitivity.Oncotarget · 2018Review
- Suppressive Effects of EGCG on Cervical Cancer.Molecules (Basel, Switzerland) · 2018Review
- Telomerase Inhibitors from Natural Products and Their Anticancer Potential.International journal of molecular sciences · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigallocatechin-3-gallate (EGCG) is a component of green tea with anticancer effects that have been demonstrated in multiple types of cancer, but few reports exist concerning its effect in esophageal squamous cell carcinoma cells. The present study investigated apoptosis induced by EGCG treatment and the underlying molecular mechanisms in Eca109 and Ec9706 human esophageal squamous cell carcinoma cells. The apoptosis rate following treatment with various concentration of EGCG for 24 h was detected by flow cytometry. The effect of EGCG on esophageal cancer cell viability was detected via MTT assay. Mitochondrial membrane potential and caspase-3 protein expression was detected in Eca109 and Ec9706 cells following treatment with EGCG by flow cytometry. The telomerase activity of Eca109 and Ec9706 cells following treatment with EGCG was assayed using the polymerase chain reaction-telomeric repeat amplification protocol (PCR-TRAP) argentation method. EGCG was demonstrated to inhibit the viability of Eca109 and Ec9706 cells in a dose-and time-dependent manner. The flow cytometry results revealed that EGCG treatment induced apoptosis, decreased the mitochondrial membrane potential and increased caspase-3 protein expression levels. PCR-TRAP argentation analysis revealed that EGCG inhibited telomerase activity. The results of the present study suggested that EGCG functions as an antitumor agent in esophageal cancer cells. The induction of apoptosis may be a viable method for treating esophageal cancer. It is possible to induce apoptosis by modulating the expression level of telomerase activity, mitochondrial membrane potential and caspase-3 protein expression levels.
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