Antiproliferative and apoptotic activites of Pylaiella littoralis extract in HT-29 cells

Abstract

Most antitumor agents induce apoptosis. Apoptosis plays an important role in physiological process as to regulate the homoeostasis through cell proliferation, differentiation, survival and death in healthy tissues. This study confirmed that five tumorigenic cells, AGS, DU145, SK-HEP, NCI-H1299 and HT-29 cells were treated with Pylaiella littoralis extract (PLE) to determine anti-proliferative activity. PLE showed anti-proliferative activities in the tested tumorgenic cells ranged from 20.2% to 67.9%. The highest inhibitory activity showed in HT-29 cells and exhibited no cytotoxic effect with increasing concentration for normal cells and inhibited cell growth of HT-29 cells depending on concentration and time. Also, we identified that growth inhibition rate on HT-29 cells of PLE was associated by as nuclear condensation, apoptotic body formation, DNA fragmentation and sub-G1 DNA accumulation in HT-29 cells. Thus, we next focused on identifying the cellular mechanisms whereby PLE induced apoptosis in HT-29 cells. PLE induced increase of mitochondrial membrane permeabilization compare with untreated PLE and exhibited decreasing Bcl-2 protein, increasing Bax protein, activating Caspase-3 and PARP expressions via caspases pathway. Indeed, PLE increased expression of phosphorylation of JNK, P38 and ERK and attenuated specific inhibitors of JNK, P38 and ERK via MAPKs pathway. In conclusion, this study demonstrated that PLE five tumorigenic cells, AGS, DU145, SK-HEP, NCI-H1299 and HT-29 cells were treated with Pylaiella littoralis extract (PLE) to determine anti-proliferative activity. PLE showed anti-proliferative activities in the tested tumorgenic cells ranged from 20.2% to 67.9%. The highest inhibitory activity showed in HT-29 cells and exhibited no cytotoxic effect with increasing concentration for normal cells and inhibited cell growth of HT-29 cells depending on concentration and time. Also, we identified that growth inhibition rate on HT-29 cells of PLE was associated by as nuclear condensation, apoptotic body formation, DNA fragmentation and sub-G1 DNA accumulation in HT-29 cells. Thus, we next focused on identifying the cellular mechanisms whereby PLE induced apoptosis in HT-29 cells. PLE induced increase of mitochondrial membrane permeabilization compare with untreated PLE and exhibited decreasing Bcl-2 protein, increasing Bax protein, activating Caspase-3 and PARP expressions via caspases pathway. Indeed, PLE increased expression of phosphorylation of JNK, P38 and ERK and attenuated specific inhibitors of JNK, P38 and ERK via MAPKs pathway. In conclusion, this study demonstrated that PLE