AIM:To evaluate the possibility of the induction of anti-tumor immune response by transfecting the colorectal cancercells with chemokine MCP-3 gene.METHODS:Mouse MCP-3 gene was transduced into mousecolorectal cancer cells CMT93 by using of Liposome.G418-resistant clones were selected and the MCP-3 mRNAexpression was detected by RT-PCR.The chemotacticactivity of MCP-3 in the cell culture supernatant wasdetected by Chemotaxis assay.The tumorigenicity of wildtype CMT93 and CMT93 gene transfectants were detectedby/n v/vo experiments.The immune cell infiltrations intumor tissue and tumor metastasis were detectedhistopathologically.RESULTS:MCP-3 mRNA expression was detected by RT-PCR in gene-transfected cells(CMT93/MCP-3),but not incontrol groups.And MCP-3 secreted in the cell culturesupernatant possessed chemotatic activity.The results fromin vivo experiments showed that the tumorigenicity ofCMT93/MCP-3 had not decreased,but the tumors derivedfrom CMT93/MCP-3 cells grew more slowly than thosefrom CMT93 cells(1.021±0.253)cm~2 vs(1.769±0.371)cm~2,P<0.05)or CMT93/mock cells(1.021±0.253)cm~2 vs(1.680±0.643)cm~2,P<0.05).Histophathological results showed fewimmune cells infiltrating in the tumor tissue derived fromthe controls.In the tumor tissue derived from CMT93/MCP-3,infiltrating immune cells increased.In addition,no tumormetastasis was found in all mice inoculated with CMT93/MCP-3 tumor cells.But all mice had tumor metastasis inCMT93 controls and 4 in 5 mice had tumor metastasis inCMT93/mock controls.CONCLUSION:The results suggested that the transfectionof chemokine MCP-3 gene could promote the induction ofanti-colorectal cancer immunity,but the tumor growth couldnot be inhibited completely by merely MCP-3 genetransfection. AIM: To evaluate the possibility of the induction of transfected the colorectal cancer cells with chemokine MCP-3 gene. METHODS: Mouse MCP-3 gene was transduced into mouse colorectal cancer cells CMT93 by using of Liposome. G418-resistant clones were selected and the MCP-3 mRNA expression was detected by RT-PCR. The chemotacticactivity of MCP-3 in the cell culture supernatant wasdetected by Chemotaxis assay. The tumorigenicity of wildtype CMT93 and CMT93 gene transfectants were detected by / nv / Cell infiltrations of tumor tissues and tumor metastasis were detected histopathologically .RESULTS: MCP-3 mRNA expression was detected by RT-PCR in gene-transfected cells (CMT93 / MCP-3), but not incontrol groups. possessed chemotatic activity. The results from in vivo experiments showed that the tumorigenicity of CMT93 / MCP-3 had not decreased, but the tumors derived from CMT93 / MCP-3 cells grew more slowly than tho There were no significant differences in CMT93 / mock cells (1.021 ± 0.253) cm ~ 2 vs (1.680 ± 0.643) cm ~ 2, P <0.05 vs CMT93 cells (1.021 ± 0.253 vs 2.769 ± 0.371 cm ~ 0.05). Histophathological results showed fewimmune cells infiltrating in the tumor tissue derived from the controls. The tumor tissue derived from CMT93 / MCP-3, infiltrating immune cells increased. In addition, no tumor metastasis was found in all mice inoculated with CMT93 / MCP- 3 tumor cells. All mice had tumor metastasis in CMT93 controls and 4 in 5 mice had tumor metastasis in CMT93 / mock controls. CONCLUSION: The results suggested that the transfection of chemokine MCP-3 gene could promote the induction of anti-colorectal cancer immunity, but the tumor growth could not be be completely completely by MCP-3 genetransfection.