Objective： We investigated the relationship between the expression of Caspase-3, cell proliferation and apoptosis in gastric cancer and their precancerous lesions, to explore the tumorigenesis of the stomach mucosa. Methods： Caspase- 3 expression in 13 normal gastric mucosa, 6 chronic atrophic gastritis （CAG）, 31 intestinal metaplasia （IM）, 114 dysplasia （DYS） and 20 gastric carcinomas were investigated immunohistochemically. Cell proliferation was evaluated with anti-Ki-67 immunostaining and apoptosis was evaluated using DNA fragmentation in situ by TdT-mediated dUTP biotin nick end labeling （TUNEL） method. Results： Caspase-3 mild-moderately positive expression was observed in most of normal superficial epithelia, its positively polar distribution in normal mucosa, CAG, IM, DYS and gastric carcinomas changed as seen in TU- NEL, and so did the positive rate. Caspase-3 protein expression showed significantly positive correlation with the number of apoptotic cells labeled with TUNEL （correlation coefficient r = 0,94; P 〈 0101）. Ki-67 expression showed a negative but not significant correlation trend with Caspase-3 （correlation coefficient r = -0.23; P 〉 0.05）. Conclusion： Caspase-3 protein expression was up-regulated from CAG to IM and mild-moderate atypical dysplasia, but down-regulated in severe dysplasia and gastric carcinoma, indicating that inactivity or reduced expression of Caspase-3 is closely correlated with carcinogenesis of the stomach mucosa.
