TROPICAL SEAWEED Pylaiella littoralis INDUCES APOPTOSIS THROUGH MITOCHONDRIAL PATHWAYS IN HT-29 CELLS AND EXERTS ANTITUMOR EFFECTS

Abstract

This study demonstrated that Pylaiella littoralis extract (PLE) in FSM could inhibit the proliferation of tumor cells. PLE showed anti-proliferative activities in the tested tumorgenic cells ranged from 20.2% to 67.9%. The highest inhibitory activity of HT-29 cells was selected for use in further experiments. PLE exhibited no cytotoxic effect in normal cells and inhibited cell growth in HT-29 cells depending on concentration and time. The results showed typical morphological characteristics of apoptosis, such as apoptotic body formation and DNA fragmentation in the PLE treated HT-29 cells. In addition, PLE induced mitochondria membrane potential depolarization and resulted increase of mitochondrial membrane permeabilization compare with untreated PLE. These results lead to decreased Bcl-2 protein, increased Bax protein, activatied Caspase-3 and PARP expressions via caspases pathway. Also, PLE increased expression of phosphorylation of JNK, P38 and ERK and attenuated specific inhibitors of JNK, P38 and ERK via MAPKs pathway.y activity of HT-29 cells was selected for use in further experiments. PLE exhibited no cytotoxic effect in normal cells and inhibited cell growth in HT-29 cells depending on concentration and time. The results showed typical morphological characteristics of apoptosis, such as apoptotic body formation and DNA fragmentation in the PLE treated HT-29 cells. In addition, PLE induced mitochondria membrane potential depolarization and resulted increase of mitochondrial membrane permeabilization compare with untreated PLE. These results lead to decreased Bcl-2 protein, increased Bax protein, activatied Caspase-3 and PARP expressions via caspases pathway. Also, PLE increased expression of phosphorylation of JNK, P38 and ERK and attenuated specific inhibitors of JNK, P38 and ERK via MAPKs pathway.