title: Effects of FasL expression in oral squamous cell cancer.
abstract: OBJECTIVE
  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 tumor infiltrating lymphocytes (TIL), and 11 cases of metastatic lymph nodes by immunohistochemistry. Apoptosis of tumor cells and TIL was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL). FasL-induction of T cell apoptosis was tested by co-culture assay in vitro with SCC-9 and 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 the same time, the positive rate of FasL significantly increased in OSCC (P<0.05) especially those with lymph node metastasis (P<0.05). The positive rates of Fas in well and middle differentiated OSCC were higher than those in poor differentiated OSCC (P<0.05). The AI of tumor cells in Fas-positive OSCC was remarkably higher than that in Fas-negative OSCC (P<0.01), with a positive correlation between Fas expression and cell differentiation as well as apoptosis (r=0.68, P<0.01). The AI of tumor cells in FasL positive OSCC was remarkably lower than that in control while the AI of TIL was higher than in FasL negative OSCC (P< 0.05). The AI of tumor cells reversely correlated with that of TIL (r = -0. 72, P<0.05). It was found that SCC-9 cells expressing functional FasL could induce apoptosis of Jurkat cells as demonstrated by co-culture assays. As a conclusion, it is evident that OSCC cells expressing FasL can induce apoptosis in Fas-expressing T cells.
  
  
  CONCLUSIONS
  In progression of OSCC, expression of the Fas/FasL changes significantly. The results suggest that FasL is a mediator of immune privilege in OSCC and may serve as an marker for predicting malignant change in oral tissues.
authors.affiliation: Stomatologic Hospital and College, Anhui Medical University, Key Lab. of Oral Diseases Research of Anhui Province, Hefei, China.
authors.forename: Li
authors.initials: L
authors.lastname: Fang
authors.forename: Lin
authors.initials: L
authors.lastname: Sun
authors.forename: Fang-Fang
authors.initials: FF
authors.lastname: Hu
authors.forename: Qiao-Er
authors.initials: QE
authors.lastname: Chen
mesh_terms: D017209:Apoptosis; D002294:Carcinoma, Squamous Cell / Q000276:immunology / Q000378:metabolism* / Q000556:secondary; D016022:Case-Control Studies; D002454:Cell Differentiation; D016009:Chi-Square Distribution; D018920:Coculture Techniques; D004848:Epithelium / Q000276:immunology / Q000378:metabolism; D053222:Fas Ligand Protein / Q000378:metabolism*; D006801:Humans; D019169:Jurkat Cells; D008207:Lymphatic Metastasis; D016246:Lymphocytes, Tumor-Infiltrating; D009061:Mouth Mucosa / Q000276:immunology / Q000378:metabolism*; D009062:Mouth Neoplasms / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D016176:T-Lymphocyte Subsets; D019014:fas Receptor / Q000378:metabolism
chemical_list: C491901:FAS protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D019014:fas Receptor