BACKGROUND: Comparative studies of cytotoxicity of docetaxel against both oral normal and tumor cells are limited. In the present study, the cytotoxicity of docetaxel towards human oral squamous cell carcinoma (OSCC) cell lines (HSC-2, HSC-3, HSC-4) and human oral normal cells (gingival fibroblasts, pulp cells, periodontal ligament fibroblasts) was investigated. MATERIALS AND METHODS: The cytotoxicity was determined by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide method. Apoptosis induction was monitored by caspase-3/7 activation, DNA fragmentation, and production of annexin-positive cells, and necrosis induction by production of propidium iodide-positive cells. RESULTS: Docetaxel induced various apoptotic markers without loss of the mitochondrial membrane potential and then necrosis markers. When the cells were rinsed with serum-free medium, the cell viability of OSCCs significantly declined. Fetal bovine serum was then fractionated by stepwise ultrafiltration. The growth-promoting activity of fetal bovine serum was heat-stable, and recovered from the fraction >100 kDa. Rinsing with serum-free medium also enhanced the cytotoxicity of docetaxel. CONCLUSION: The present results suggest that docetaxel may induce apoptosis via a mitochondrial-independent pathway and rinsing of target cells or organs with serum-free medium may reduce the clinical dose of docetaxel and its side effects.
BACKGROUND: Comparative studies of cytotoxicity of docetaxel against both oral normal and tumor cells are limited. In the present study, the cytotoxicity of docetaxel towards humanoral squamous cell carcinoma (OSCC) cell lines (HSC-2, HSC-3, HSC-4) and human oral normal cells (gingival fibroblasts, pulp cells, periodontal ligament fibroblasts) was investigated. MATERIALS AND METHODS: The cytotoxicity was determined by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide method. Apoptosis induction was monitored by caspase-3/7 activation, DNA fragmentation, and production of annexin-positive cells, and necrosis induction by production of propidium iodide-positive cells. RESULTS:Docetaxel induced various apoptotic markers without loss of the mitochondrial membrane potential and then necrosis markers. When the cells were rinsed with serum-free medium, the cell viability of OSCCs significantly declined. Fetal bovine serum was then fractionated by stepwise ultrafiltration. The growth-promoting activity of fetal bovine serum was heat-stable, and recovered from the fraction >100 kDa. Rinsing with serum-free medium also enhanced the cytotoxicity of docetaxel. CONCLUSION: The present results suggest that docetaxel may induce apoptosis via a mitochondrial-independent pathway and rinsing of target cells or organs with serum-free medium may reduce the clinical dose of docetaxel and its side effects.