B7-H1 expression and its contribution to the regulation of biological function in human esophageal cancer cell line

Objective To study the impact of downregulating the negative costimulation molecule B7-H1 on biological behaviors in esophageal cancer cell line Eca-109. Methods Down-regulation of B7-H1 was performed by using RNAi method in the human esophageal cancer cell line Eca-109. The expression level of B7-H1 was confirmed by using flow cytometry and Western blotting. The cell counting kit-8 (CCK-8) assay, scratch assay and Transwell assay were used to investigate the contribution of B7-H1 to biological behaviors of esophageal cancer cells. Results We successfully constructed stably reduced expression of B7-H1 in human esophageal cancer cell line by using RNAi named Eca109-B7-H1-small interfering RNA (siRNA) and the control group Eca109-NC. The CCK-8 cell proliferation experiment showed that on the day 6, 7 and 8, the proliferation rate in Eca109-B7-H1-siRNA group (0.61±0.03, 0.78±0.04, and 0.89±0.04) was significantly lower than in the control group (0.80±0.01, 1.00±0.04, and 1.07±0.09; P 0.05). The scratch assay results revealed that the cell migration ability in Eca109-B7-H1-siRNA group [(126.00±22.63) μm was significantly reduced as compared with the control group [(339.00±22.11) μm] at 24 h (P 0.05). Transwell invasion assay results demonstrated that at 24 h after the cells were seeded, the number of invasive cells in Eca109-B7-H1-siRNA group [(20.60±4.61) cells] was singnificantly less than in the control group [(60.40±12.50) cells, P<0.01]. Conclusion Down-regulation of B7-H1 in esophageal cancer cell line Eca-109 could significantly inhibit the cell proliferation, migration and invasion, suggesting that the abnormal expression of B7-H1 in esophageal carcinoma cells could be involved in regulating the tumor biological behaviors and contribute to the tumor progression. Key words: B7-H1; Esophageal cancer; Eca-109; RNA interference