Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis in Ec9706 and Eca109 esophageal carcinoma cells

Liu,Liang; Zuo,Jing; Wang,Guangda

doi:10.3892/ol.2017.6712

Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis in Ec9706 and Eca109 esophageal carcinoma cells

Authors:
- Liang Liu
- Jing Zuo
- Guangda Wang
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Affiliations: Department of Flow Cytometry Analysis, Tumor Institute, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China
Published online on: August 3, 2017 https://doi.org/10.3892/ol.2017.6712
Pages: 4391-4395

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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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