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JING Shao-wu, WANG Ya-di, WU Feng-peng, LU Fu-he, HAN Chun, LIU Qing, CHENG Yun-jie. Radiosensitivity and Its Mechanism of Arsenic Trioxide on Esophageal Cancer Cell Line-Eca109[J]. Cancer Research on Prevention and Treatment, 2011, 38(06): 620-623. DOI: 10.3971/j.issn.1000-8578.2011.06.003
Citation: JING Shao-wu, WANG Ya-di, WU Feng-peng, LU Fu-he, HAN Chun, LIU Qing, CHENG Yun-jie. Radiosensitivity and Its Mechanism of Arsenic Trioxide on Esophageal Cancer Cell Line-Eca109[J]. Cancer Research on Prevention and Treatment, 2011, 38(06): 620-623. DOI: 10.3971/j.issn.1000-8578.2011.06.003

Radiosensitivity and Its Mechanism of Arsenic Trioxide on Esophageal Cancer Cell Line-Eca109

  • ObjectiveTo explore the effects of Arsenic trioxide (As2O3) and As2O3 combined with radiation on the growth inhibition of esophageal cancer cell line-Eca109. To analysis the impact of As2O3 combined with radiation on the cell cycle and apoptosis in order to provide a theoretical basis for As2O3 applied the treatment of esophageal cancer. MethodsThe inhibitory effects of radiation or/and As2O3 on proliferation were measured by MTT assay. The straight of irradiated group, As2O3 group and combined group were fitted by linear correlation and linear regression and then sensitizing enhancement ratio (SER) was calculated. The change of cell cycle distribution and apoptosis were assayed by flow cytometry. The effects of As2O3 combined with radiation on manganese superoxide dismutase (MnSOD) and cytochrome C (cyt-C) expression were measured by Western blot. ResultsWith a clear dose and time effect, As2O3 could inhibit the proliferation of esophageal cell line-Eca109; As2O3 definitely enhanced radiosensitivity of Eca109 cells.Flow cytometry analysis results indicated that G2/M phase proportion and apoptosis rate increased obviously after the effect of As2O3 and radiation. The expression of MnSOD was down-regulated, while cyt-C had no obvious change. ConclusionAs2O3 could enhance radiation's killing effect on Eca109 cells through G2/M phase arrest, down-regulation of MnSOD and induction of apoptosis.
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