Abstract: Objective To investigate the mechanism of cisplatin-induced damage in the esophageal cancer cell line ECA109. Methods The proliferation with different time and concentrations of cisplatin was determined by MTT assay in ECA109 cells, the cell growth curve was drawn, and the low concentration drug，which be used in subsequent experiments，was selectd。The cisplatin induced nuclear foci (IF) average number changes of r-H2AX, P-STAT1 and CHK2-T68 at 24 h in 50 ECA109 cells were detected by immunofluorescence. The cisplatin induced nucleus foci (IF) average number changes of r-H2AX, P-STAT1 and CHK2-T68 at 24 h in 50 ECA109 cells were determined by immunofluorescence before and after silence H2AX gene or STAT1 respectively. Results The inhibition of proliferation induced by cisplatin in ECA109 cells were time and dose-dependent. Cisplatin can induce ECA109 cells to produce r-H2AX, P-STAT1 and CHK2-T68 nucleus foci (P<0.05). Cisplatin-induced r-H2AX, P-STAT1 and CHK2-T68 nucleus foci were reduced through silence H2AX gene, P<0.05. Cisplatin-induced P-STAT1 within CHK2-T68 nuclear foci were reduced by silence STAT1 gene (P<0.05). Conclusions Cisplatin can induce esophageal cancer cell injury, resulting in a variety of nuclear foci. In this damage response, H2AX is at the top regulating STAT1 and CHK2; STAT1 located downstream of H2AX and upstream of CHK2, adjusting CHK2.

Key words: Esophageal cancer, cisplatin, Damage response, Nuclear foci