OBJECTIVETo study whether As(2)O(3) has an apoptotic effect on human solid tumor cells, and the possible cellular and molecular mechanisms of this treatment using human esophageal squamous carcinoma cells (EC8712) as a model.

METHODSDNA microarray, biochemical and cytological analyses were used.

RESULTSThe growth and survival of EC8712 cells were markedly inhibited by As(2)O(3) treatment at a concentration of 1, 2 and 4 micromol/L. EC8712 cells were obviously arrested at G2/M phase with As(2)O(3) treatment and apoptosis induced at micromolar As(2)O(3) concentrations, as shown by morphology, histogram related nuclear DNA contents, and DNA gel electrophoresis. As(2)O(3) activated caspase-3, which might be involved in the process of As(2)O(3), induced apoptosis in EC8712 cells.

CONCLUSIONSAs(2)O(3) changes the expression of many genes at transcription level. The regulation of expression of many genes might be involved in the process of As(2)O(3) inducing apoptosis. These results suggest that As(2)O(3) can be clinically useful for solid tumor treatment.

Apoptosis ; drug effects ; Arsenicals ; pharmacology ; Carcinoma, Squamous Cell ; drug therapy ; genetics ; pathology ; Cell Adhesion ; drug effects ; Cell Division ; drug effects ; DNA Fragmentation ; drug effects ; Dose-Response Relationship, Drug ; Esophageal Neoplasms ; drug therapy ; genetics ; pathology ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; Microscopy, Electron ; Oxides ; pharmacology ; Tumor Cells, Cultured ; drug effects ; ultrastructure