Paris Saponin I Induces G2/M Cell Cycle Arrest and Apoptosis in Human Gastric Carcinoma SGC7901 Cells

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences 2011-12, Vol.31 (6), p.768-772
• Main Authors: Xiao, Meifang, Dai, Xiahong, He, Xinchun, Zhou, Rongrong, Zhang, Baoxin, Hu, Guansheng, Huang, Zebing, Fan, Xuegong
• Format: Article
• Language: English
• Subjects: Antineoplastic Agents, Phytogenic - pharmacology; Apoptosis - drug effects; caspase; Cell Cycle Checkpoints - drug effects; Cell Division; Cell Line, Tumor; Cell Proliferation - drug effects; Diosgenin - analogs & derivatives; G2 Phase; Humans; Liliaceae - chemistry; Medicine; Medicine & Public Health; Plant Extracts - pharmacology; Saponins - pharmacology; Stomach Neoplasms - pathology; Western印迹法; 巴黎; 细胞凋亡; 细胞周期蛋白B; 细胞周期阻滞; 胃癌; 诱导凋亡
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-011-0674-y

The aim of this study was to investigate the effect of Paris saponin I （PSI ） on human gastric carcinoma cell growth and apoptosis and to explore the potential mechanisms. The proliferation of SGC7901 cells was monitored by the MTT cell viability assay, while the nuclear morphology of apoptotic cells was assessed by Hoechst 33258 staining. Flow cytometry was performed to analyze the cell cycle progression of propidium iodide （PI）-stained SGC7901 cells and the apoptotic rate of annexin V/PI-stained ceils. Western blotting was used to examine the expression of several cell cycle proteins, including cyclin 131 and Cdkl, and the apoptosis-regulated proteins Bcl-2, Bax, cytochrome c, procaspase-9, and procaspase-3. The MTT assay demonstrated that PSI could induce significant dose- and time-dependent inhibition of SGC7901 cell proliferation. Marked morphological changes, including condensation of chromatin, nuclear fragmentation and apoptotic bodies were clearly shown on Hoechst 33258 staining. PS I treatment also resulted in the disruption of the cell cycle at Gz/M and the induction of apoptosis. Following PSI treatment, the cell cycle-related proteins cyclin B 1 and Cdkl were down- regulated. Expression of the pro-apoptotic protein Bax was increased, while anti-apoptotic protein Bcl-2 decreased. PSI treatment resulted in elevated cytoplasmic cytochrome c and activation of the apoptotic proteases caspase-9 and caspase-3. These data indicate that PS I acts as an inhibitor of proliferation in SGC7901 cells by inducing cell cycle arrest and mitochondria-dependent apoptosis. PSI is a potential therapeutic agent against human gastric carcinoma.