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

Abstract

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.

Molecular Targets of Epigallocatechin—Gallate (EGCG): A Special Focus on Signal Transduction and Cancer

“…In prostate cancer cell lines, it has been observed that the EGCG-dependent reduction of the acetylated androgen receptor (AR) gene might be induced by EGCG reduction in HAT activity [65]. EGCG also acts on teleomerase, reducing its activity in different tumor types as esophageal carcinoma [230], glioma [231], cervical cancer [232], breast cancer [100], nasopharyngeal carcinoma [233], ovarian cancer [68], laryngeal squamous cell carcinoma [234], and lung cancer [235]. It has also been shown that EGCG can translocate from the cytoplasm to the nucleus where it can bind to DNA, suggesting a possible role in gene expression regulation also through the direct binding to nucleic acid [236,237].…”

Suppressive Effects of EGCG on Cervical Cancer

“…Therefore, further studies should focus on the mechanism of EGCG on depolymerizing cellular microtubule. In addition, EGCG can inhibit telomerase in breast cancer [ 117 ], esophageal carcinoma [ 118 ], endocervical cells and ectocervical cells [ 42 ], but shows much milder cytotoxic effects in cervical cancer cells [ 119 ]. The activity of telomerase is related to DNA methylation [ 120 ], and thus whether EGCG can inhibit telomerase activity through reducing DNA methylation is a promising research project.…”

Telomerase Inhibitors from Natural Products and Their Anticancer Potential

“…EGCG is a naturally occurring polyphenol from the catechin group found in tea (green, white and black), fruits (apples and plums), vegetables (onions and carobs) and nuts (hazelnuts and pecans). EGCG possibly induces apoptosis and telomerase inhibition activity, and provokes mitochondrial membrane potential and caspase-3 expression in various cancer cells [ 215 , 216 , 217 ]. In addition, EGCG has down-regulated the mRNA and protein expression of hTERT and c-Myc protein [ 218 ].…”

“…Low cytotoxic dose EGCG and (−)-epigallocatechin (EGC) have suppressed hTERT expression on reporter system and hTERT mRNA level in various cancers [ 213 , 214 ]. Liu et al [ 217 ] reported that EGCG induces apoptosis by down-regulating hTERT and B cell lymphoma 2 (Bcl-2), arresting cells in both G2/M and S phase and promoting DNA damage response specifically in ovarian cancer cell lines.…”