| BACKGROUND and OBJECTIVE: The regulation of apoptosis, a distinctive form of programmed cell death, in multistep Barrett's esophagus (BE) carcinogenesis is poorly understood. The aim of this study was to explore the pathogenesis and investigate the role of apoptosis and apoptosis-related proteins Bcl-2 and P53 in the development of Barrett's esophagus and esophageal adenocarcinoma (EA).METHODS: The apoptotic index (AI) and the expression of apoptosis-related proteins of Bcl-2 and P53 were studied in normal esophageal squamous epithelium (n=20), BE (n=50) and EA (n=25) by TUNEL method and immunohistochemical staining assay respectively. The differences among the three groups were compared and the correlations were analyzed.RESULTS:⑴Apoptotic index (AI) of EA was higher than that of normal esophageal squamous epithelium and BE (P<0.01). AI of BE was higher than that of normal esophageal squamous epithelium, but the difference between them had not a statistical significance.⑵The expression of Bcl-2 protein in BE and EA was more than that in normal esophageal squamous epithelium (P<0.01). Moreover, an increasing tendency was observed from normal esophageal squamous epithelium to BE and EA (rs =0.406,P<0.01). Positive staining lied in cytoplasm, cell membrane or karyotheca.⑶The expression level of P53 protein was low in normal esophageal squamous epithelium, in contrast to high expression in BE and EA (P<0.01). Moreover, we also observed an increasing tendency in the three groups(rs =0.621,P<0.01). Positive staining region was in cell nucleus.⑷In BE and EA, a negative correlation (rs=-0.507,P<0.01) between Bcl-2 expression and AI was found. Simultaneously, a negative correlation (rs=-0.660, P<0.01) between P53 expression and AI was found.⑸Along with increase of the cell differentiation level of esophageal adenocarcinoma, apoptotic index decreased (rs =0.483,P <0.05), whereas the expression of Bcl-2 protein (rs=-0.586,P<0.01)and P53(rs=-0.793,P<0.01)increased.CONCLUSIONS: Inhibition of apoptosis may make an impact on the course of the occurrence of BE and its progress to esophageal adenocarcinoma. Bcl-2 and mutant P53 may contribute to carcinogenesis of Barrett's esophageal cells by inhibiting apoptosis. |
