Objective:To investigate the effect of KISS1 gene suppression on the metastatic capacity of the human colorectal carcinoma cells HCT116 and the involvement of protein kinase C signaling pathway. Methods:p GC-LV-KISS1-EGFP lentiviral vector was constructed and the colorectal cancer cells HCT116 was infected and divided into :the point blank control group（CON）

the noncarrier contral group（NC）and the over-expression group（OE）. q RT-PCR and Western blot methods were used to detect KISS1 gene product m RNA and Metastin level

the key molecular of PKC signaling pathway PKCα

PKCβ Ⅱ and E-cadherin sticky protein expression. Transwell Chambers methods were used to detect the changes of cell ’s invasion and migration ability. Results:After lentiviral transfection

HCT-116 cells could stably express EGFP report gene

and the fluorescence rate was over 80%. Compare with those of the CON and NC

the KISS1 gene product m RNA and Metastin level of the OE were significantly increased. The protein expression of PKCβ Ⅱ（0.288 2±0.023 7）was significantly increased compared with that of the CON（0.530 9±0.013 3）and NC（0.511 7±0.008 5

P<0.05）. But the protein expression of PKCα had no significant change（P>0.05）. The E-cadherin expression level（0.633 2±0.017 4）rose highly compared with that of the CON（0.232 2±0.019 6）and NC（0.252 3±0.018 2）with statistical significances（P<0.05）. The cell’s invasion

migration ability of the OE group also significantly decreased compared with that of the other two groups（P<0.05）. Conclusion:KISS1 gene may regulate the PKCβⅡ and raise the E-cadherin sticky protein expression and plays a role of inhibiting the invasion and migration in the HCT116

which will become a new target for the prevention and treatment of colorectal cancer metastasis.