Jin Ha Lee, Doman Kim, Young-Hwan Moon, Yeon-Jin Jeong, Kyung-Joo Seong, Hoi-Soon Lim, Sun-Hun Kim, Won-Jae Kim, Ji-Yeon Jung
Abstract
(−)-Epigallocatechin-3-gallate (EGCG) has been reported to inhibit cellular proliferation and induce apoptosis in a range of cancer cells. This study examined the cytotoxicity of EGCG glucoside on human laryngeal epidermoid carcinoma Hep2 cells. The EGCG glucoside treatment decreased the cell viability in Hep2 cells. Furthermore, EGCG glucoside caused apoptotic morphological changes with chromatin condensation and nuclear fragmentation, as observed by a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and activated caspase-3 immunohistochemisty. However, the EGCG glucoside did not induce the production of reactive oxygen species (ROS), suggesting that oxidative stress is not involved in the apoptotic response. EGCG glucoside induces apoptosis in Hep2 cells through not the generation of ROS, but the activation of caspase-3.
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