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

[摘要] 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; theD0andDqvalues 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 were15.9±0.57%,42.7±0.37%,19.9±0.48%, and41.5±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 were16.7±0.67%,30.1±0.95%,26.7±0.62%, and36.3±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.

[学科分类] 基础医学