Ethyl acetate extract of Nepenthes adrianii x clipeata induces antiproliferation, apoptosis, and DNA damage against oral cancer cells through oxidative stress

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...

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Bibliographic Details
Published in:Environmental toxicology 2019-08, Vol.34 (8), p.891-901
Main Authors: Tang, Jen‐Yang, Peng, Sheng‐Yao, Cheng, Yuan‐Bin, Wang, Chun‐Lin, Farooqi, Ammad Ahmad, Yu, Tzu‐Jung, Hou, Ming‐Feng, Wang, Sheng‐Chieh, Yen, Chia‐Hung, Chan, Leong‐Perng, Ou‐Yang, Fu, Chang, Hsueh‐Wei
Format: Article
Language:English
Subjects:
Acetates
Acetic acid
Acetylcysteine
Adenosine diphosphate
ADP
Annexin V
Anticancer properties
Antitumor activity
Apoptosis
Cancer
Cell cycle
Cell viability
Damage
Deoxyribonucleic acid
Disruption
DNA
DNA damage
Ethyl acetate
ethyl acetate extract
Flow cytometry
Herbal medicine
Medicinal plants
Membrane potential
Mitochondria
Nepenthes
Nepenthes plants
Oral cancer
Oxidative stress
Plant cells
Plant extracts
Poly(ADP-ribose) polymerase
Pretreatment
Reactive oxygen species
Ribose
Superoxide
Traditional Chinese medicine
Western blotting
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Summary: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 IC50 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.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22748