|
 |
|||||||||||||||||||
|
|||||||||||||||||||
|
|||||||||||||||||||
 |
 |
|
|
Enhancement of Cisplatin-Induced Apoptosis and Caspase 3 Activation by Depletion of Mitochondrial DNA in a Human Osteosarcoma Cell Line
aGraduate Institute of Medical Biotechnology and School of Medical Technology, Chang Gung University, Tao-Yuan, Taiwan bDepartment of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
Address for correspondence: Hsiu-Chuan Yen, Ph.D., Graduate Institute of Medical Biotechnology, Chang Gung University, 259 Wen-Hwa 1st Rd., Kwei-Shan, Tao-Yuan 333, Taiwan. Voice: +886-3-2118800 ext. 5207; fax: +886-3-2118692. yen{at}mail.cgu.edu.tw
Cisplatin is an anticancer drug that can induce apoptosis. In this study, we investigated the effect of mitochondrial DNA (mtDNA) depletion on cisplatin-induced cell death using a human osteosarcoma cell line (143B) and mtDNA-depleted 143B cells (143B-
 0). Results showed that cisplatin decreased cell survival in 143B-0 cells. Moreover, cisplatin induced a greater extent of apoptosis-associated DNA fragmentation and caspase 3 activation in 143B-0 cells. The release of mitochondrial cytochrome c into cytosol by cisplatin was enhanced more obviously in 143B cells than in 143B-0 cells; however, in the control group of 143B-0 cells, it was already dramatically greater. Depletion of mtDNA may increase sensitivity of cells to cisplatin-induced apoptosis by enhancing caspase 3 activation via both cytochrome c-dependent and -independent pathways.
Key Words: cisplatin • mitochondrial DNA • apoptosis • caspase 3 • cytochrome c This article has been cited by other articles:
| |||||||||||||||||||||||||||||
 |
 |
