Cepharanthine induces apoptosis through reactive oxygen species and mitochondrial dysfunction in human non-small-cell lung cancer cells.

Abstract

Cepharanthine is a medicinal plant-derived natural compound which possesses potent anti-cancer properties. However, there is little report about its effects on lung cancer cells. In this study, we investigated the effects of cepharanthine on the cell viability and apoptosis in human non-small-cell lung cancer H1299 and A549 cells. It was found that cepharanthine inhibited the growth of H1299 and A549 cells in a dose-dependent manner which was associated with the generation of reactive oxygen species(ROS) and the dissipation of mitochondrial membrane potential (Δψm). These effects were markedly abrogated when cells were pretreated with N-acetylcysteine (NAC), a specific ROS inhibitor, indicating that the apoptosis-inducing effect of cepharanthine in lung cancer cells was mediated by ROS. In addition, cepharanthine triggered apoptosis in non-small lung cancer cells via the upregulation of Bax, downregulation of Bcl-2 and significant activation of caspase-3 and PARP. These results provide the rationale for further research and preclinical investigation of cepharanthine's anti-tumor effect against human non-small-cell lung cancer.

• Authors: Peiyan Hua, Mei Sun, Guangxin Zhang, Yifan Zhang, Xin Tian, Xin Li, Ranji Cui, Xingyi Zhang
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 460 Issue 2 Pg. 136-42 (May 01 2015) ISSN: 1090-2104 [Electronic] United States
• PMID: 25747710 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015 Elsevier Inc. All rights reserved.

Chemical References

• Benzylisoquinolines
• Reactive Oxygen Species
• cepharanthine
• Acetylcysteine

Topics

• Acetylcysteine (pharmacology)
• Apoptosis (drug effects)
• Benzylisoquinolines (pharmacology)
• Carcinoma, Non-Small-Cell Lung (metabolism, pathology, physiopathology)
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Humans
• Lung Neoplasms (metabolism, pathology, physiopathology)
• Membrane Potential, Mitochondrial (drug effects)
• Reactive Oxygen Species (metabolism)