Chikusetsu (CHI) triggers mitochondria-regulated apoptosis in human prostate cancer via reactive oxygen species (ROS) production

• Published in: Biomedicine & pharmacotherapy 2017-06, Vol.90, p.446-454
• Main Authors: Zhu, Wen-bin, Tian, Fu-jun, Liu, Li-qian
• Format: Article
• Language: English
• Subjects: Apoptosis; Apoptosis - drug effects; Apoptosis Inducing Factor - metabolism; Caspases - metabolism; Cell Line, Tumor; Cell Proliferation - drug effects; Chikusetsu saponin Iva; Endodeoxyribonucleases - metabolism; Humans; Internal Medicine; Male; Medical Education; Mitochondria - drug effects; Mitochondria - metabolism; Oleanolic Acid - analogs & derivatives; Oleanolic Acid - pharmacology; Prostate cancer; Prostatic Neoplasms - drug therapy; Prostatic Neoplasms - metabolism; Reactive Oxygen Species - metabolism; ROS; Saponins - pharmacology; Signal Transduction - drug effects
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/j.biopha.2017.03.050

Abstract The prostate cancer prognosis is still not fully understood. Chikusetsu saponin Iva (CHI), isolated from Aralia taibaiensis , shows anti-cancer and anti-inflammatory properties. Here, in our study, we attempted to explore the efficiency and the possible molecular mechanism by which CHI may suppress prostate cancer. CHI was found to inhibit prostate cancer cell proliferation and induce cell death without cytotoxicity in prostate normal cells. CHI resulted in intracellular reactive oxygen species (ROS) production, and induced apoptosis regulated by mitochondria in vitro studies. CHI-caused apoptosis was shown in both caspase-dependent and −independent manner, which released cyto-c, enhancing caspases expression and promoting apoptosis-inducing factors (AIF) as well as endonuclease G (Endo G) nuclear transfer, respectively. Moreover, in vivo study showed that prostate tumor was inhibited by CHI administration through apoptosis induction. Thus, the results illustrated that CHI might be an effective therapeutic strategy for prostate cancer treatment in future.