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eCAM Advance Access published online on January 8, 2009
eCAM, doi:10.1093/ecam/nen084
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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.

Cordycepin Induced MA-10 Mouse Leydig Tumor Cell Apoptosis through Caspase-9 Pathway

Chun-Yi Jen1,*, Chun-Yu Lin1,*, Sew-Fen Leu2 and Bu-Miin Huang1

1Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China and 2Institute of Bioindustrial Technology, College of Human Ecology, HungKuang University, Taichung, Taiwan, Republic of China

In the present study, the apoptotic effect of cordycepin on MA-10 cells, a mouse Leydig tumor cell line, was investigated. Results demonstrated that the number of rounding-up cell increased by cordycepin (10 µM to 5 mM for 24 h), and cells with plasma membrane blebbing could be observed by 100 µM cordycepin. In viability test, MA-10 cell surviving rate significantly decreased as the dosage (10 µM to 5 mM) and duration (3–24 h) of cordycepin treatment increased (P < 0.05). Cordycepin at 100 µM and 1 mM for 24 h treatment induced significant DNA fragmentation (P < 0.05). In addition, the percentage of G1 and G2/M phase cell significantly declined by cordycepin (100 µM and 1 mM) for 24 h treatment, while the percentages of subG1 phase cell increased by 100 µM and/or 1 mM cordycepin in 6, 12 and 24 h treatments (P < 0.05), respectively, which highly suggested that cordycepin induced MA-10 cell apoptosis. In mechanism study with the treatments of caspases, c-Jun NH2 terminal kinase (JNK) or reactive oxygen species (ROS) inhibitors plus cordycepin for 24 h, only caspases inhibitor suppressed subG1 phase in MA-10 cells. Moreover, western blotting results showed that cordycepin induced caspase-9, -3 and -7 protein expressions, but not caspase-8, in time- and dose-dependent manners. In conclusion, cordycepin induced apoptosis in MA-10 mouse Leydig tumor cells through a caspase-9 and -3 and -7 dependent pathway.

Keywords: Apoptosis – cordycepin – caspase – MA-10 – mouse – Leydig

For reprints and all correspondence: Bu-Miin Huang, Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, #1 University Road, Tainan, 701, Taiwan, Republic of China. Tel: 886-6-208-9357; Fax: 886-6-209-3007; E-mail: bumiin{at}mail.ncku.edu.tw

Sew-Fen Leu, Ph.D. Institute of Bioindustrial Technology, College of Human Ecology, HungKuang University, #34 Chung-Chie Rd, Sha Lu, Taichung, 443, Taiwan, Republic of China. Tel: 886-4-2631-8652 ext 5072; Fax: 886-4-2631-7591; E-mail: sfleu{at}sunrise.hk.edu.tw.

*These authors contribute equally to this work

Received August 27, 2008; accepted December 5, 2008


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