MS-5, a Naphthalene Derivative, Induces the Apoptosis of an Ovarian Cancer Cell CAOV-3 by Interfering with the Reactive Oxygen Species Generation.
10.4062/biomolther.2018.020
- Author:
Eunsook MA
1
;
Seon Ju JEONG
;
Joon Seok CHOI
;
Thi Ha NGUYEN
;
Chul Ho JEONG
;
Sang Hoon JOO
Author Information
1. Department of Pharmacy, Daegu Catholic University, Gyeongsan 38430, Republic of Korea. sjoo@cu.ac.kr
- Publication Type:Original Article
- Keywords:
Reactive oxygen species;
Apoptosis;
Anti-cancer effect
- MeSH:
Adenosine Triphosphate;
Apoptosis*;
Biological Processes;
Blotting, Western;
Cell Line;
Cell Survival;
Flow Cytometry;
G1 Phase Cell Cycle Checkpoints;
Membrane Potential, Mitochondrial;
Metabolism;
Ovarian Neoplasms*;
Phytochemicals;
Reactive Oxygen Species*;
Superoxides
- From:Biomolecules & Therapeutics
2019;27(1):48-53
- CountryRepublic of Korea
- Language:English
-
Abstract:
Reactive oxygen species (ROS) are widely generated in biological processes such as normal metabolism and response to xenobiotic exposure. While ROS can be beneficial or harmful to cells and tissues, generation of ROS by diverse anti-cancer drugs or phytochemicals plays an important role in the induction of apoptosis. We recently identified a derivative of naphthalene, MS-5, that induces apoptosis of an ovarian cell, CAOV-3. Interestingly, MS-5 induced apoptosis by down-regulating the ROS. Cell viability was evaluated by water-soluble tetrazolium salt (WST-1) assay. Apoptosis was evaluated by flow cytometry analysis. Intracellular ROS (H₂O₂), mitochondrial superoxide, mitochondrial membrane potential (MMP) and effect on cycle were determined by flow cytometry. Protein expression was assessed by western blotting. The level of ATP was measured using ATP Colorimetric/Fluorometric Assay kit. MS-5 inhibited growth of ovarian cancer cell lines, CAOV-3, in a concentration- and time-dependent manner. MS-5 also induced G1 cell cycle arrest in CAOV-3 cells, while MS-5 decreased intracellular ROS generation. In addition, cells treated with MS-5 showed the decrease in MMP and ATP production. In this study, we found that treatment with MS-5 in CAOV-3 cells induced apoptosis but decreased ROS level. We suspect that MS-5 might interfere with the minimum requirements of ROS for survival. These perturbations appear to be concentration-dependent, suggesting that MS-5 may induce apoptosis by interfering with ROS generation. We propose that MS-5 may be a potent therapeutic agent for inducing apoptosis in ovarian cancer cell through regulation of ROS.
