Original Article
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Oct 21, 2011; 17(39): 4389-4395
Published online Oct 21, 2011. doi: 10.3748/wjg.v17.i39.4389
Paris chinensis dioscin induces G2/M cell cycle arrest and apoptosis in human gastric cancer SGC-7901 cells
Lin-Lin Gao, Fu-Rong Li, Peng Jiao, Ming-Feng Yang, Xiao-Jun Zhou, Yan-Hong Si, Wen-Jian Jiang, Ting-Ting Zheng
Lin-Lin Gao, Yan-Hong Si, Department of Pathology and Pathophysiology, Taishan Medical University, Taian 271000, Shandong Province, China
Fu-Rong Li, School of Pharmaceutical Science, Taishan Medical University, Taian 271000, Shandong Province, China
Peng Jiao, Ming-Feng Yang, Institute of Basic Medical Sciences, Taishan Medical University, Taian 271000, Shandong Province, China
Xiao-Jun Zhou, Wen-Jian Jiang, Ting-Ting Zheng, Department of Clinical Medicine, Taishan Medical University, Taian 271000, Shandong Province, China
Author contributions: Gao LL and Jiao P performed the majority of experiments; Gao LL and Li FR designed the research; Zhou XJ, Si YH, Zheng TT and Jiang WJ participated in cell culture and part of laser scanning confocal microscopic detection; Yang MF analyzed the data of the detection results; Li FR and Jiao P provided the vital reagents and analytical tools and were involved in editing the manuscript; Gao LL and Li FR edited the manuscript; Li FR and Jiao P analyzed the data.
Supported by The grant from the Department of Education of Shandong Province, China, No. J10LF18
Correspondence to: Lin-Lin Gao, MD, Department of Pathology and Pathophysiology, Taishan Medical University, No. 2, Yingshengdong Road, Taian 271000, Shandong Province, China. ytgd98@yahoo.cn
Telephone: +86-538-6225010 Fax: +86-538-6222036
Received: February 14, 2011
Revised: May 6, 2011
Accepted: May 13, 2011
Published online: October 21, 2011
Abstract

AIM: To investigate the anti-tumor effects of Paris chinensis dioscin (PCD) and mechanisms regarding cell cycle regulation and apoptosis in human gastric cancer SGC-7901 cells.

METHODS: Cell viability was analyzed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. Cell apoptosis was evaluated by flow cytometry and laser scanning confocal microscope (LSCM) using Annexin-V/propidium iodide (PI) staining, and the cell cycle was evaluated using PI staining with flow cytometry. Intracellular calcium ions were detected under fluorescence microscope. The expression of cell cycle and apoptosis-related proteins cyclin B1, CDK1, cytochrome C and caspase-3 was measured by immunohistochemical staining.

RESULTS: PCD had an anti-proliferation effect on human gastric cancer SGC-7901 cells in a dose- and time-dependent manner. After treatment of SGC-7901 cells with PCD, apoptosis appeared in SGC-7901 cells. Morphological changes typical of apoptosis were also observed with LSCM by Annexin V/PI staining, and the cell number of the G0/G1 phase was decreased, while the number of cells in the G2/M phase was increased. Cell cycle-related proteins, such as cyclin B1 and CDK1, were all down-regulated, but caspase-3 and cytochrome C were up-regulated. Moreover, intracellular calcium accumulation occurred in PCD-treated cells.

CONCLUSION: G2/M phase arrest and apoptosis induced by PCD are associated with the inhibition of CDK-activating kinase activity and the activation of Ca2+-related mitochondrion pathway in SGC-7901 cells.

Keywords: CyclinB1/CDK1, Cell cycle arrest, Caspase-3, Ca2+, Cytochrome C