BACKGROUND AND OBJECTIVE: Previous studies have shown that Bmi-1 is 
overexpressed in a variety of tumors, suggesting that Bmi-1 plays an important 
role in tumorigenesis. In this study, we investigated the effect of Bim-1 siRNA 
on cell proliferation, cell cycle, cell apoptosis and migration of human 
esophageal carcinoma EC9706 cells, and explored its potential mechanisms.
METHODS: Bmi-1 small interfering RNA (siRNA) was transferred into EC9706 cells. 
Then, cell proliferation was measured using cell counting kit-8 (CCK-8), cell 
cycle and cell apoptosis were analyzed by flow cytometry, cell migration ability 
was detected using Boyden chamber assay, and the mRNA and protein expression 
levels of Bmi-1, p16, Bcl-2, Bax, and MMP-2 were determined using real-time 
polymerase chain reaction (PCR) and Western blot analysis, respectively.
RESULTS: Bmi-1 siRNA treatment significantly inhibited the expression of Bmi-1 
at both mRNA and protein levels in EC9706 cells. Cell proliferation rate 
decreased dramatically in the Bmi-1 siRNA treated group than in the untreated 
group and in the scrambled siRNA treated group (both P < 0.001). In Bmi-1 
treated group, the percentage of cells at G(0)/G(1) stage was 71.93%, which was 
higher than that in the untreated group (47.36%) or scramble siRNA treated group 
(48.47%) (both P < 0.001). Early cell apoptosis rate also increased 
significantly in the Bmi-1 siRNA treated group (both 17.32%) than in the 
untreated group (2.61%) and in the scramble siRNA treated group (2.73%) (both P 
< 0.001). Further experiment suggested that downregulation of Bmi-1 led to less 
cell migration. In EC9706 cells transfected by Bmi-1 siRNA, the expression 
levels of p16 and Bax increased, while the expression level of Bcl-2 decreased.
CONCLUSIONS: Bmi-1 downregulation in esophageal carcinoma cells inhibits cell 
proliferation, cell cycle, and cell migration, while increases cell apoptosis. 
These results suggest that Bmi-1 is a potential molecular target of treating 
esophageal cancer.