Alteration of proto-oncogenes during apoptosis in the oral squamous cell carcinoma cell line, SAS, induced by staurosporine.

Staurosporine (ST) has been reported to induce apoptosis in many kinds of cultured cells. The pathway of the apoptosis induced by ST is still not clear. Certain proto-oncogene expressions have been shown to be involved in the apoptotic pathway. The present study characterized apoptosis induced by ST in the oral squamous cell carcinoma cell line, SAS, focusing on the alteration of proto-oncogene expression. SAS showed typical apoptotic features upon exposure to ST. We compared the level of gene expression in apoptosis induced by ST with that by withdrawal of serum, which is a common system to induce apoptosis. By RT-PCR analysis, ST-induced apoptosis showed c-fos and c-jun up-regulation, whereas serum withdrawal-induced apoptosis showed c-jun up-regulation and the same levels of p21/waf-1 and c-myc. These results indicate that ST can rapidly induce apoptosis in SAS, possibly via a c-fos and c-jun pathway.

Pattern of expression of beta-defensins in oral squamous cell carcinoma.

Human beta-defensin (hBD)-1 and hBD-2 are antimicrobial peptides that have been detected in certain types of epithelia, including the skin and oral epithelia. It has been suggested that bacterial infection is an important factor in the process of carcinogenesis. The expression of hBDs in oral squamous cell carcinoma (SCC) may be down-regulated. We studied the pattern of expression of hBD-1 and hBD-2 mRNA in oral (SCC) cell lines and in tumor samples obtained from four patients with oral SCC who underwent surgical resection, by reverse transcription-polymerase chain reaction (RT-PCR). Human gingival epithelial (HGE) cells were used as the control. The effect of various inflammatory cytokines on hBD-1 and hBD-2 expression in the HGE cells and SCC cell lines, was also studied. hBD-1 mRNA was detected in the Ca-9, SCC-9 and HSC-4 cell lines, but not in the SAS and KB cell lines. hBD-2 mRNA was detected in all five cell lines. All four tumor samples expressed both hBD-1 and hBD-2 mRNA, although the mRNA level of each protein varied. These results indicate that SCCs in which hBD expression is downregulated, may be susceptible to bacterial infection.

Loss of essential membrane lipids and ascorbic acid from rat brain following cryogenic injury and protection by methylprednisolone.

Previous work has shown that unsaturated fatty acid components of model membrane phospholipids in vitro, damaged via a free radical mechanism, are protected by the presence of cholesterol in these membranes. The participation of these membrane lipids in the pathogenesis of traumatic injury to brain was studied in vivo using the Klatzo method of cryogenic injury in rats. Increased edema 4 hr after cryogenic injury was noted on the lesioned side. Total cerebral cholesterol was decreased significantly in the lesioned hemispheres 10 hr following injury. In lesioned animals pretreated and post-treated with methylprednisolone, there were no significant differences in the cholesterol levels. Arachidonic acid isolated from total membrane phospholipids was significantly reduced on the injured side 24 hr after injury, but not before. Other fatty acids were not significantly affected. Methylprednisolone treatment prevented the decrease in arachidonic acid. Animals that had received a cold injury had significant decreases in ascorbic acid levels after 4 hr on the lesioned side of the brain. This decrease was significantly ameliorated by corticosteroid administration. These results support the hypothesis that the protective effect of corticosteroids in cryogenic cerebral trauma may be due to antioxidant protection of major cell membrane lipid components such as cholesterol and phospholipids.