Wnt signaling pathway is important for development and carcinogenesis. 
Alterations of this pathway, such as mutations in adenomatous polyposis coli 
(APC) gene and activation mutations of beta-catenin, would result in 
stabilization of beta-catenin and subsequent translocation to nucleus where 
genes are transcribed. Recently, a receptor of Wnt, FzE3 was found to be 
up-regulated in esophageal carcinoma while a non-receptor antagonist of Wnt, 
secreted frizzled related protein (hsFRP) was found to be down-regulated in some 
cancer. These findings suggested that FzE3 is a potential oncogene while hsFRP 
is a potential tumor suppressor gene. We aimed to investigate whether FzE3 and 
hsFRP were altered in gastric cancer. Twelve cases of gastric cancer, including 
7 cases of intestinal type, 4 cases of diffuse type and I case of mixed type, 
were studied. FzE3 and hsFRP mRNAs were expressed in most of the paired normal 
gastric tissues. FzE3 was over-expressed in 9 cases (75%) of gastric carcinoma 
tissues while hsFRP was down-regulated in 2 cases (16%). Beta-catenin nuclear 
staining was identified in 3 cases (27%) and cyclin D1 was expressed in 5 cases 
(41%) of cancer samples. All these cases were associated with either 
up-regulation of FzE3 or down-regulation of hsFRP. Our results suggested that 
alterations of FzE3 or hsFRP were frequent in gastric cancer. These provide 
alternative mechanisms leading to activation of Wnt signaling pathway in gastric 
carcinogenesis.