AIM:To study the role of Fas ligand (FasL) and Caspase-3expression in carcinogenesis and progression of gastriccancer and molecular mechanisms of relevant immuneescape.METHODS:Fasl and Caspase-3 expression was studiedin adjacent epithelial cells,cancer cells and lymphocytesof primary foci,and cancer cells of metastatic foci from113 cases of gastric cancer by streptavidin-biotin-peroxidase(S-P) immunohistochemistry.Expression of both proteinsin cancer cells of primary foci was compared withclinicopathological features of gastric.cancer.The relationshipbetween FasL expression in cancer cells and Caspase-3expression in cancer cells or infiltrating lymphocytes ofprimary foci was investigated.RESULTS:Cancer cells of primary foci expressed Fasl in53.98% (61/113) of gastric cancers,more than their adjacentepithelial cells (34.51%,39/113) (P=0.003,X~2=8.681),whilethe expression of Caspase-3 in cancer cells of primary fociwas detected in 32.74% (37/113) of gastric cancers,lessthan in the adjacent epithelial cells (50.44%,57/113)(P=0.007,X~2=7.286).Infiltrating lymphocytes of the primaryfoci showed positive immunoreactivity to Caspase-3 in70.80% (80/113) of gastric cancers,more than theircorresponding adjacent epithelial cells (P=0.001,X~2=10.635)or cancer cells of primary foci (P=0.000,X~2=32.767).FasLwas less expressed in cancer cells of metastases (51.16%,22/43) than in those of the corresponding primary foci(81.58%,31/38) (P=0.003,X~2=9.907).Conversely,Caspase-3 was more expressed in cancer cells of metastases(58.14%,25/43) than in those of the corresponding primaryfoci (34.21%,13/38) (P=0.031,X~2=4.638).FasL expressionwas significantly correlated with tumor size (P=0.035,rs=0.276),invasive depth (P=0.039,rs=0.195),metastasis(P=0.039,rs=0.195),differentiation (P=0.015,rs=0.228)and Lauren’s classification (P=0.038,rs=0.196),but not withage or gender of patients,growth pattern or TNM stagingof gastric cancer (P>0.05).In contrast,Caspase-3 expressionshowed no correlation with any clinicopathological parametersdescribed above in cancer cells of the primary foci (P>0.05).Interestingly,FasL expression in primary gastric cancer cellsparalleled to Caspase-3 expression in infiltrating lymphocytes of the primary foci (P=0.016,X~2=5.825).CONCLUSION:UP-regulated expression of FasL and down-regulated expression of Caspase-3 in eaneer cells of Primary foci Play an important role jn gastric carcjnogenesjs.As an effective marker to reveal the biologieal behaviors,FasL is implicated in differentiation,growth,invasion and metastasis of gastric cancer by inducing apoptosis of infiltrating Iymphocytes.Chemieal substances derived from the primary foci and metastatic microenvironment can inhibit the growth of metastatic cells by enhancing Caspase-3 expression and diminishing FasL expression. AIM: To study the role of Fas ligand (FasL) and Caspase-3 expression in carcinogenesis and progression of gastriccancer and molecular mechanisms of relevant immuneescape. METHODS: Fasl and Caspase-3 expression was studied in adjacent epithelial cells, cancer cells and lymphocytes of primary foci, and cancer cells of metastatic foci from 113 cases of gastric cancer by streptavidin-biotin-peroxidase (SP) immunohistochemistry. Expression of both proteins in cancer cells of primary foci was compared with clinical pathological features of gastric. Cancer. The relationship between FasL expression in cancer cells and Caspase- 3expression in cancer cells or infiltrating lymphocytes of primary foci was investigated.RESULTS: Cancer cells of primary foci expressed Fasl in53.98% (61/113) of gastric cancers, more than their adjacentepithelial cells (34.51%, 39/113) (P = 0.003, X ~ 2 = 8.681), while the expression of Caspase-3 in cancer cells of primary foci was detected in 32.74% (37/113) of gastric cancers, lessthan in the adjace nt epithelial cells (50.44%, 57/113) (P = 0.007, X ~ 2 = 7.286) .Infiltrating lymphocytes of the primaryfoci showed positive immunoreactivity to Caspase-3 in 70.80% (80/113) of gastric cancers, more than Their corresponding adjacent epithelial cells (P = 0.001, X ~ 2 = 10.635) or cancer cells of primary foci (P = 0.000, X ~ 2 = 32.767) in those of the corresponding primary foci (81.58%, 31/38) (P = 0.003, X ~ 2 = 9.907) .Conversely, Caspase-3 was more expressed in cancer cells of metastases (P = 0.035, rs = 0.276), invasive depth (P = 0.039, rs = = 0.195), metastasis (P = 0.039, rs = 0.195), differentiation (P = 0.015, rs = 0.228) and Lauren’s classification (P = 0.038, rs = 0.196), but not withage or gender of patients, growth pattern or TNM staging of gastric cancer (P> 0.05) .In contrast, Caspase-3 expressionshowed no correlation with any clinicopathological parametersdescribed above in cancer cells of the primary foci (P> 0.05) .Interestingly, FasL expression in primary gastric cancer cellsparalleled to Caspase-3 expression in infiltrating lymphocytes of the primary foci (P = 0.016, X ~ 2 = .CONCLUSION: UP-regulated expression of FasL and down-regulated expression of Caspase-3 in eaneer cells of Primary foci Play an important role jn gastric carcjnogenesj. As an effective marker to reveal the biologie behaviors, FasL is implicated in differentiation, growth, invasion and metastasis of gastric cancer by inducing apoptosis of infiltrating Iymphocytes. Chemieal substances derived from the primary foci and metastatic microenvironment can inhibit the growth of metastatic cells by enhancing Caspase-3 expression and diminishing FasL expression.