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Apoptotic Response of Human Oral Squamous Carcinoma Cells to Etoposide  

Kim, Gyoo-Cheon (Dept. of Oral Anatomy, College of Dentistry and Research Institute for Oral Biotechnology, Pusan National University)
Lee, Kyoung-Duk (Dept. of Oral Anatomy, College of Dentistry and Research Institute for Oral Biotechnology, Pusan National University)
Park, Jae-Hyun (Dept. of Oral Anatomy, College of Dentistry and Research Institute for Oral Biotechnology, Pusan National University)
Kim, Duk-Han (Dept. of Oral Anatomy, College of Dentistry and Research Institute for Oral Biotechnology, Pusan National University)
Park, Jeong-Kil (Dept. of Oral Conserve dentistry, College of Dentistry and Research Institute for Oral Biotechnology, Pusan National University)
Park, June-Sang (Dept. of Oral Medicine, College of Dentistry and Research Institute for Oral Biotechnology, Pusan National University)
Park, Bong-Soo (Dept. of Oral Anatomy, College of Dentistry and Research Institute for Oral Biotechnology, Pusan National University)
Publication Information
Journal of Oral Medicine and Pain / v.30, no.2, 2005 , pp. 231-238 More about this Journal
Abstract
Anti-cancer drugs have been shown to target diverse cellular functions in mediation cell death in chemosensitive tumors. Most antineoplastic drugs used in chemotherapy of leukemias and solid tumors induce apoptosis in drug-sensitive target cells. However, the precise molecular requirements that are central for drug-induced cell death are largely unknown. Etoposide is used for the treatment of lung and testicular cancer. This study was performed to examine whether etoposide promote apoptosis in human oral squamous carcinoma cells (OSC9) as well as in lung and testicular cancer. Etoposide had a significant dose- and time-dependent inhibitory effect on the viability of OSC9 cells. TUNEL assay showed the positive reaction on condensed nuclei. Hoechst stain demonstrated that etoposide induced a change in nuclear morphology. The expression of p53 was increased at 48 hour, suggesting that the nuclear of OSC9 cell was damaged, thereby inducing apoptosis. Etoposide treatment induced caspase-3 cleavage and activation. Intact PARP protein 116-kDa and 85-kDa cleaved product were observed. The activated caspase-3 led cleavage of the PARP. These results demonstrate that etoposide-induced apoptosis in OSC9 cells is associated with caspase-3 activation.
Keywords
Apoptosis; etoposide; human oral squamous carcinoma cells;
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