APC pathway including beta-catenin, c-MYC, and pS2 protein in intestinal type of stomach cancer

A proposal that in normal colorectal epithelial cells, the adenomatous polyposis coli gene (APC) might modulate directly c-MYC transcription through beta-catenin/Tcf-4 was reported in 1998 (1-4). It was reported that intestinal trefoil factor (TTF) which is the same family of pS as a gastric specific tumor suppressor gene (5) is related to beta-catenin (6). Therefore, to elucidate the applicability of APC pathway in stomach and relationship between this pathway and pS2, the expressions of pS2, c-MYC, and beta-catenin proteins was evaluated by immunohistochemically in 30 cases of intestinal carcinoma of stomach which is morphologically close to colon cancer. Their immunoreactivities were 56.7% for pS2, 43.3% for c-MYC, and 86.7% for beta-catenin proteins. Interestingly, positive staining of. beta-catenin showed heterogenous pattern according to depth of invasion. Tumor cells in the invading or infiltrating edges shows strong positivity, while the tumor cells in mucosa showed loss of the expression in even same tumors. These results can indicate that in intestinal carcinoma of stomach beta-catenin involves tumor cell migration and invasion not as cell adhesion molecule but as tumor-suppressor molecule forming complex with APC.