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Study on the effects of B7-H3 down-regulation on cell cycle and apoptosis of lung cancer A549 cells
Pages: 193-198
Year: Issue:  3
Journal: International Journal of Radiation Medicine and Nuclear Medicine

Abstract: Objective To explore the effects of B7-H3 down-regulation on cell cycle and apoptosis in lung cancer A549 cells.Method Human lung cancer cell line A549 were cultured.siB7-H3 RNA which can specifically silence the expression of B7-H3 protein was transfected into A549 cells.137Cs γ-ray irradiation was used with a single dose of 4 Gy.Experiments included control group,siB7-H3 transfected group,irradiation group,and irradiation+siB7-H3 transfected group.After transfected with siB7-H3,Western blotting and quantitative real-time PCR assays were used to detect the expression of B7-H3 protein and mRNA in A549 cells.The cell cycle and apoptosis of A549 cells following 4 Gy irradiation were detected by flow cytometry.Results The protein and mRNA expression of B7-H3 were significantly decreased in A549 cells transfected with siB7-H3 compared with the control group,and the differences between the two groups were statistically significant (t =-4.222,P=0.013).siB7-H3 transfection induced significant effect on cell cycle with increase of G0/G1 phase arrest and reduction of S and G2/M phase population.A mild enhanced G0/G1 phase arrest and an obvious enhanced G2/M phase arrest of irradiation group were detected compared with the control group.An enhanced G0/G1 and G2/M phase arrest of irradiation+siB7-H3 transfected group were detected compared with the control group.Compared with the control group,the necrosis and apoptosis induction of the irradiated group significantly increased at 48 h after irradiation.However,No significant alterations of necrosis and apoptosis induction were observed between irradiation group and irradiation+ siB7-H3 transfected group.Conclusions Down-regulation of B7-H3 can significantly elevated the G0/G1 arrest in A549 cells following radiation.This conclusion indicated that the alteration of B7-H3 expression could play a key role in the regulation of the radiosensitivity of lung cancer via mediating the G0/G1 check point.
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