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eCAM Advance Access first published online on April 21, 2009
This version published online on May 25, 2009
eCAM, doi:10.1093/ecam/nep016
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© 2009 The Author(s).
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Aqueous Extract of Shi-Liu-Wei-Liu-Qi-Yin Induces G2/M Phase Arrest and Apoptosis in Human Bladder Carcinoma Cells via Fas and Mitochondrial Pathway

Ting-Tsz Ou1,*, Chau-Jong Wang1, Guang-Uei Hung2,*, Cheng-Hsun Wu3 and Huei-Jane Lee1

1Institute of Biochemistry and Biotechnology, College of Medicine, Chung Shan Medical University, Taichung, 2Department of Nuclear Medicine, Chang Bing Show Chwan Memorial Hospital, Changhua and 3Department of Anatomy, China Medical University, No. 91, Hsueh-Shih Road, Taichung, Taiwan

Shi-Liu-Wei-Liu-Qi-Yin (SLWLQY) was traditionally used to treat cancers. However, scientific evidence of the anticancer effects still remains undefined. In this study, we aimed to clarify the possible mechanisms of SLWLQY in treating cancer. We evaluated the effects of SLWLQY on apoptosis-related experiments inducing in TSGH-8301 cells by (i) 3-(4,5-dimethylthiazol-zyl)-2,5-diphenylterazolium bromide (MTT) for cytotoxicity; (ii) cell-cycle analysis and (iii) western blot analysis of the G2/M-phase and apoptosis regulatory proteins. Human bladder carcinoma TSGH-8301 cells were transplanted into BALB/c nude mice as a tumor model for evaluating the antitumor effect of SLWLQY. Treatment of SLWLQY resulted in the G2/M phase arrest and apoptotic death in a dose-dependent manner, accompanied by a decrease in cyclin-dependent kinases (cdc2) and cyclins (cyclin B1). SLWLQY stimulated increases in the protein expression of Fas and FasL, and induced the cleavage of caspase-3, caspase-9 and caspase-8. The ratio of Bax/Bcl2 was increased by SLWLQY treatment. SLWLQY markedly reduced tumor size in TSGH-8301 cells-xenografted tumor tissues. In the tissue specimen, SLWLQY up-regulated the expression of Fas, FasL and Bax proteins, and down-regulated Bcl2 as well as in in vitro assay. Our results showed that SLWLQY reduced tumor growth, caused cell-cycle arrest and apoptosis in TSGH-8301 cells via the Fas and mitochondrial pathway.

Keywords: apoptosis – G2/M-phase arrest – human bladder carcinoma cells – SLWLQY

For reprints and all correspondence: Dr Huei-Jane Lee, Institute of Biochemistry and Biotechnology, College of Medicine, Chung Shan Medical University, No. 110, Sec. 1, Jianguo N. Road, Taichung 402, Taiwan. Tel: +886-4-24730022; Fax: +886-4-23248195; E-mail: lhj{at}csmu.edu.tw

*These authors contributed equally to this work

The original version was published with the wrong affiliation for co-author, Guang-Uei Hung.

Received September 23, 2008; accepted January 28, 2009


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