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We observed the effects of endostar on the radiosensitivity of pulmonary adenocarcinoma A549 cells and found that endostar inhibited A549 cell growth under normoxia and hypoxia in time and dose-dependent manners; the D0 and Dq values in control and endostar groups were (1.36 and 1.30) versus (1.019 and 1.015) under normoxia and (1.693 and 1.39) versus (2.453 and 1.026) under hypoxia, respectively; SER was 1.04 under normoxia and 1.22 under hypoxia in endostar group; under normoxia, the apoptosis rates in control, radiotherapy, endostar and combination groups were 15.9±0.57%, 42.7±0.37%, 19.9±0.48%, and 41.5±0.38%, respectively, with no significant difference between combination and radiotherapy groups; there was significant difference in G2/M phase cells between combination and radiotherapy groups (P=0.028); under hypoxia, the apoptosis rates in the four groups were 16.7±0.67%, 30.1±0.95%, 26.7±0.62%, and 36.3±0.71%, respectively, with significant difference between combination and radiotherapy groups; G2/M phase cells were higher in combination group than radiotherapy group (P=0.000); G2/M phase cells were higher in hypoxic combination group than in normoxic combination group (P=0.003). Based on these results, we conclude that under hypoxia, endostar can enhance the radiosensitivity of A549 cells through G2/M arrest.

Enhancement of Recombinant Human Endostatin on the Radiosensitivity of Human Pulmonary Adenocarcinoma A549 Cells and Its Mechanism