Objective： To investigate the change of the cell cycle, apoptosis and radiosensitivity effect by COCl2 induced hypoxia in esophageal cancer line Eca109 cells in vitro. Methods： The hypoxia culture model induced by 1...Objective： To investigate the change of the cell cycle, apoptosis and radiosensitivity effect by COCl2 induced hypoxia in esophageal cancer line Eca109 cells in vitro. Methods： The hypoxia culture model induced by 150 microM COCl2 was established. The cell cycle and apoptosis were measured with flow cytometry （FCM）. The radiosensitivity was analysized with clonogenic assay after irradiation alone or combined with hypoxia in Eca109 cells in vitro. Results： Eca109 cells were treated with 150 microM COCl2 for 24 h, cell cycle arrest in G0/G1 phase increase and decreasing arrest in S phase with longer of hypoxiac time （0-24 h）, the other rate of cell cycle and apoptosis did not change obviously. The G2/M phase block was arrested obviously in radiation alone comparing with the hypoxia plus irradiated group, apoptosis did not occur in Eca109 cell line following irradiation. The DO value and cell surviving fraction of Eca109 cell was 2.48 Gy, 2.44 Gy and 97.33%, 96.33% in hypoxia and control group, respectively; the Dq value of Eca109 cell was 2.89 Gy, 0.52 Gy, the cell surviving fraction after radiation with 4 Gy was 48.3%, 21.7% in hypoxia and control group, respectively. The hypoxia decreased the radiosensitivity in esophageal cancer Eca109 cells with clonogenic assay. Conclusion： Hypoxia induced by COCl2 influences radiosensitivity of Eca109 cell through regulating cellular proliferation rates.展开更多
基金the Tackle Key Problems in Science andTechnology of Hebei Province (No. 052761764)
文摘Objective： To investigate the change of the cell cycle, apoptosis and radiosensitivity effect by COCl2 induced hypoxia in esophageal cancer line Eca109 cells in vitro. Methods： The hypoxia culture model induced by 150 microM COCl2 was established. The cell cycle and apoptosis were measured with flow cytometry （FCM）. The radiosensitivity was analysized with clonogenic assay after irradiation alone or combined with hypoxia in Eca109 cells in vitro. Results： Eca109 cells were treated with 150 microM COCl2 for 24 h, cell cycle arrest in G0/G1 phase increase and decreasing arrest in S phase with longer of hypoxiac time （0-24 h）, the other rate of cell cycle and apoptosis did not change obviously. The G2/M phase block was arrested obviously in radiation alone comparing with the hypoxia plus irradiated group, apoptosis did not occur in Eca109 cell line following irradiation. The DO value and cell surviving fraction of Eca109 cell was 2.48 Gy, 2.44 Gy and 97.33%, 96.33% in hypoxia and control group, respectively; the Dq value of Eca109 cell was 2.89 Gy, 0.52 Gy, the cell surviving fraction after radiation with 4 Gy was 48.3%, 21.7% in hypoxia and control group, respectively. The hypoxia decreased the radiosensitivity in esophageal cancer Eca109 cells with clonogenic assay. Conclusion： Hypoxia induced by COCl2 influences radiosensitivity of Eca109 cell through regulating cellular proliferation rates.
