Basic Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Mar 21, 2016; 22(11): 3186-3195
Published online Mar 21, 2016. doi: 10.3748/wjg.v22.i11.3186
Melittin induces human gastric cancer cell apoptosis via activation of mitochondrial pathway
Gui-Mei Kong, Wen-Hua Tao, Ya-Li Diao, Peng-Hua Fang, Ji-Jun Wang, Ping Bo, Feng Qian
Gui-Mei Kong, Wen-Hua Tao, Peng-Hua Fang, Ji-Jun Wang, Ping Bo, Feng Qian, Department of Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Medical School of Yangzhou University, Yangzhou 225001, Jiangsu Province, China
Ya-Li Diao, Department of Gastroenterology, 1st Hospital of Yangzhou, Yangzhou 225009, Jiangsu Province, China
Author contributions: Kong GM and Tao WH contributed equally to this work; Bo P and Qian F designed the research; Kong GM, Tao WH and Diao YL performed the research; Tao WH, Fang PH and Wang JJ analyzed the data; and Kong GM wrote the paper.
Supported by the Natural Science Foundation of China, No. 30801497, No. 81272537 and No. 81472815; and the Natural Science Fund for Colleges and Universities in Jiangsu Province, No. 11KJD360003.
Institutional review board statement: The study was reviewed and approved by the medical school of Yangzhou University Institutional Review Board.
Institutional animal care and use committee statement: This article does not include animal trials.
Conflict-of-interest statement: To the best of our knowledge, no conflict of interest exists.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Feng Qian, MD, Department of Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Medical School of Yangzhou University, No. 88 Road, Yangzhou 225001, Jiangsu Province, China. amawy@126.com
Telephone: +86-514-87978872 Fax: +86-514-87341733
Received: September 5, 2015
Peer-review started: September 6, 2015
First decision: November 5, 2015
Revised: November 17, 2015
Accepted: December 12, 2015
Article in press: December 12, 2015
Published online: March 21, 2016
Core Tip

Core tip: SGC-7901 cells stimulated by melittin displayed typical apoptotic morphology. In addition, reactive oxygen species release was induced, and the mitochondrial membrane permeability was rendered irreversibly open, causing a reduction in the mitochondrial membrane potential. These changes increased the release of cytochrome C, apoptosis-inducing factor, and endonuclease G and decreased second mitochondria-derived activator of caspases (Smac)/direct IAP binding protein with low isoelectric point (Diablo), which activated downstream caspase-3 and induced apoptosis.