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Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress
Author(s) -
Tang JenYang,
Peng ShengYao,
Cheng YuanBin,
Wang ChunLin,
Farooqi Ammad Ahmad,
Yu TzuJung,
Hou MingFeng,
Wang ShengChieh,
Yen ChiaHung,
Chan LeongPerng,
OuYang Fu,
Chang HsuehWei
Publication year - 2019
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22748
Subject(s) - oxidative stress , apoptosis , reactive oxygen species , viability assay , cancer cell , dna damage , biology , flow cytometry , poly adp ribose polymerase , annexin , microbiology and biotechnology , cancer , biochemistry , pharmacology , chemistry , dna , polymerase , genetics
Abstract Nepenthes plants are regarded as a kind of Traditional Chinese Medicine for several diseases but its anticancer activity remain unclear. The subject of this study is to evaluate the antiproliferation effects on oral cancer cells by Nepenthes plants using ethyl acetate extract of Nepenthes adrianii x clipeata (EANA). Cell viability was detected using MTS assay. Its detailed mechanisms including cell cycle, apoptosis, oxidative stress, and DNA damage were explored by flow cytometry or western blotting. For 24 hours EANA treatment, five kinds of oral cancer cells (CAL 27, Ca9‐22, OECM‐1, HSC‐3, and SCC9) show IC 50 values of cell viability ranging from 8 to 17 μg/mL but the viability of normal oral cells (HGF‐1) remains over 80%. Subsequently, CAL 27 and Ca9‐22 cells with high sensitivity to EANA were chosen to investigate the detailed mechanism. EANA displays the time course and concentration effects for inducing apoptosis based on flow cytometry (subG1 and annexin V analyses) and western blotting [cleaved poly (ADP‐ribose) polymerase (c‐PARP)]. Oxidative stress and DNA damage were induced by EANA treatments in oral cancer cells through reactive oxygen species (ROS), mitochondrial membrane potential disruption, mitochondrial superoxide, and γH2AX. All these changes of EANA treatments in oral cancer cells were reverted by the ROS scavenger N ‐acetylcysteine pretreatment. Therefore, EANA induces preferential killing, apoptosis, and DNA damage against oral cancer cells through oxidative stress.