title: Effects of alpha fetoprotein on escape of Bel 7402 cells from attack of lymphocytes.
abstract: BACKGROUND
  Involvement of AFP against apoptosis of tumor cell has been implicated in its evasion of immune surveillance. However, the molecular events of immune escape mechanisms are still unknown. The major observations reported here relate to a possible mechanism by which heptoloma Bel 7402 cells escape immune surveillance in vitro.
  
  
  METHODS
  Western blotting and a well-characterized cofocal scanning image were performed to analyze the expression of Fas/FasL and caspase-3 in co-cultured Bel 7402 and Jurkat cells.
  
  
  RESULTS
  After co-culture with Jurkat cells, up-regulated Fas and reduced FasL expression could be observed. Treatment with AFP could remarkably inhibit the elevated Fas and, whereas, induce the FasL expression in co-cultured Bel 7402 cells. Cells co-culture could induce the expression of caspase-3 in both cells line. The elevated caspase-3 in Bel 7402 cells was abolished following the treatment of AFP. The expression of caspase-3 was elevated in co-cultured Jurkat cells treated with AFP. No detectable change on the expression of survivin was examined in both cells line. Monoclonal antibody against AFP treatment alone did not obviously influence the growth of cells, as well as the expression of Fas/FasL and caspase-3. However, the effect of AFP could be blocked by antibody.
  
  
  CONCLUSIONS
  our results provide evidence that AFP could promote the escape of liver cancer cells from immune surveillance through blocking the caspase signal pathway of tumor cells and triggering the Fas/FasL interaction between tumor cells and lymphocytes.
authors.affiliation: Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100083, China. ligang55@263.net
authors.forename: Mengsen
authors.initials: M
authors.lastname: Li
authors.forename: Xinhua
authors.initials: X
authors.lastname: Liu
authors.forename: Sheng
authors.initials: S
authors.lastname: Zhou
authors.forename: Pingfeng
authors.initials: P
authors.lastname: Li
authors.forename: Gang
authors.initials: G
authors.lastname: Li
mesh_terms: D000911:Antibodies, Monoclonal / Q000737:chemistry; D015153:Blotting, Western; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D018920:Coculture Techniques; D053222:Fas Ligand Protein; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins; D019169:Jurkat Cells; D008214:Lymphocytes / Q000378:metabolism* / Q000473:pathology; D008562:Membrane Glycoproteins / Q000378:metabolism; D018613:Microscopy, Confocal; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009363:Neoplasm Proteins / Q000378:metabolism; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction; D000077022:Survivin; D048069:Tumor Necrosis Factors / Q000378:metabolism; D000509:alpha-Fetoproteins / Q000378:metabolism / Q000502:physiology*; D019014:fas Receptor / Q000096:biosynthesis
chemical_list: D000911:Antibodies, Monoclonal; C107489:BIRC5 protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; D051034:Inhibitor of Apoptosis Proteins; D008562:Membrane Glycoproteins; D008869:Microtubule-Associated Proteins; D009363:Neoplasm Proteins; D000077022:Survivin; D048069:Tumor Necrosis Factors; D000509:alpha-Fetoproteins; D019014:fas Receptor; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases