Purpose: To probe the role of FasL in cell apoptosis in oral squamous cell carcinomas (OSCCs). Methods:The expression of Fas/FasL was assessed in 10 cases of normal oral epithelium, 38 cases of OSCC and tumorinfiltrating lymphocytes (TIL), and 11 cases of metastatic lymph nodes by immunohistochemistry. Apoptosisof tumor cells and TIL was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick endlabeling assay (TUNEL). FasL-induction of T cell apoptosis was tested by co-culture assay in vitro with SCC-9and Jurkat T cells. Results: The 10 cases of normal oral epithelium all demonstrated extensive expression of Fas,the positive rate being largely down-regulated in OSCC (21/38) (P<0.05) compared to the normal (10/10). At thesame time, the positive rate of FasL significantly increased in OSCC (P<0.05) especially those with lymph nodemetastasis (P<0.05). The positive rates of Fas in well and middle differentiated OSCC were higher than thosein poor differentiated OSCC (P<0.05). The AI of tumor cells in Fas-positive OSCC was remarkably higher thanthat in Fas-negative OSCC (P<0.01), with a positive correlation between Fas expression and cell differentiationas well as apoptosis (r=0.68, P<0.01). The AI of tumor cells in FasL positive OSCC was remarkably lower thanthat in control while the AI of TIL was higher than in FasL negative OSCC (P< 0.05). The AI of tumor cellsreversely correlated with that of TIL (r = -0. 72, P<0.05). It was found that SCC-9 cells expressing functionalFasL could induce apoptosis of Jurkat cells as demonstrated by co-culture assays. As a conclusion, it is evidentthat OSCC cells expressing FasL can induce apoptosis in Fas-expressing T cells. Conclusions: In progression ofOSCC, expression of the Fas/FasL changes significantly. The results suggest that FasL is a mediator of immuneprivilege in OSCC and may serve as an marker for predicting malignant change in oral tissues.
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