0.05), but serum levels of, SS, SP and VIP were higher than those of control group (P05). When the intensity reached 120dB, gastrointestinal transit was accelerated significantly(P

0.05), and the serum levels of MLT, SS, SP, and VIP were higher than those of control group(P0.05). When the noise was higher than 80dB, gastrointestinal transit was increased significantly (P

Objective To investigate the underlying mechnisms of Kangai-1(KAI1)gene,a tumor metastasis suppressor gene,on metastasis and prolification of pancreatic cancer cells.Methods The plasmin containing Ad-KAI1 was established and transfected into pancreatic cancer cell line PCNA Ⅰ.The PCNA Ⅰ cells were then divided into different groups according to the times induced by vascular endothelial growth factor(VEGF)and epidermal growth factor(EGF).The morphology and migrational ability of PANC Ⅰ cells were compared before and after transfection by microscopy and transwell method,respectively.The expressions of intercellular adhesion molecule-1(ICAM-1)and matrix metalloproteinases-9(MMP-9)in PANC Ⅰ cells were examined by immunocytochemistry before and after transfection.Results The migrational ability of PCNA Ⅰ cells transfected with Ad-KAI1 was siginificantly decreased compared with untransfected PCNA Ⅰ cells(P＜0.05).Immunocytochemistry study revealed that the expressions of ICAM-1 and MMP-9 were both positive in untransfected PCNA Ⅰcells,but were both negative in transfected PCNA Ⅰ cells.Conclusion The inhibitory mechanism of KAI1 gene on metastasis of pancreatic cancer is associated with down-regulation of ICAM-1 and MMP-9expressions.