Expression of Aspartic Proteinases in Gastric Cancer: An Immunohistochemical Study

Abstract

We used the immunohistochemical method to localize the aspartic proteinases, including pepsinogen Ⅰ (PG Ⅰ), pepsinogen Ⅱ (PG Ⅱ), and cathepsin E in 45 gastrectomy specimens from patients with gastric carcinoma. Positive staining for PG Ⅰ, PG Ⅱ and cathepsin E were 46.7%, 88.9% and 97.8% in normal glands or epithelial cells, and 4.4%, 26.7%, and 66.7% in cancer cells respectively. The distribution of PG Ⅱ and cathepsin E varied from diffuse to sporadic, but only a few cancer cells were positive for PG Ⅰ in 2 specimens. There was no relationship between the locations and differentiation of cancer and the positive staining of aspartic proteinases in cancer cells. Cancer without concomitant intestinal metaplasia had a higher incidence of PG Ⅱ staining than cancer with intestinal metaplasia (36.7% vs 6.6%, P=0.031). In addition, higher incidences of PG Ⅱ positive cancer cells were found in the intestinal type than in diffuse type carcinoma, with greater presence of metastasis than absence of metastasis, but their differences did not reach statistical significance. Among the 45 specimens, cancer cells were positive for the following: Cathepsin E only: 19 specimens; cathepsin E and PG Ⅱ: 9; both three aspartic proteinases: 2; PG Ⅱ only: 2. Cancer cells were negative for all three proteinases in 14 specimens. The distribution of aspartic proteinases in our gastric cancer indicated that most of those cancers arose from surface or foveolar epithelial cells, and rarely from PG Ⅰ producing cells. There is a tendency to have more PG Ⅱ staining in metastatic cancer, intestinal type adenocarcinoma and cancer not associated with intestinal metaplasia. Thus, the role of PG Ⅱ in carcinogenesis and cancer spreading needed further investigation.