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目的:研究PI3K抑制剂对食管癌细胞株Eca-109放射增敏作用及机制.方法:以食管癌细胞株Eca-109为实验对象,MTT法观察PI3K抑制剂LY294002对Eca-109细胞增殖抑制;克隆形成实验分析细胞放射敏感性;RT-PCR检测DNA双链断裂修复基因DNA-PKcs mRNA表达;流式细胞技术检测细胞周期.结果:PI3K抑制剂LY294002对Eca-109细胞有生长抑制作用,且呈剂量依赖性,在较低浓度(10μmol/L)时即可降低Eca-109细胞的克隆形成率,其放射增敏比为1.58.药物LY294002组DNA-PKcs mRNA表达受抑,但与对照组比较差异无统计学意义;照射组表达较对照组明显升高(P<0.05);药物LY294002+照射组的表达较照射组下降(P<0.05).药物LY294002组G2期细胞比例与对照组比较差异无统计学意义,照射组较对照组升高(P<0.01),药物LY294002+照射组G2期细胞比例较照射组下降(P<0.05).结论:PI3K抑制剂LY294002对Eca-109细胞有放射增敏作用,其机制可能与抑制肿瘤细胞DNA双链断裂修复基因DNA-PKcs及减少G2期细胞阻滞有关.
AIM: To investigate the radiosensitization effect of PI3K inhibitor on esophageal cancer cell line Eca-109 and its mechanism.Methods: The esophageal cancer cell line Eca-109 was used as the experimental object, and the PI3K inhibitor LY294002 was used to inhibit the proliferation of Eca-109 cells by MTT assay. The DNA-PKcs mRNA expression was detected by RT-PCR and the cell cycle was detected by flow cytometry.Results: The PI3K inhibitor LY294002 could inhibit the growth of Eca-109 cells In a dose-dependent manner, the formation rate of Eca-109 cells was reduced at a lower concentration (10μmol / L), and the radiosensitization ratio was 1.58. The expression of DNA-PKcs mRNA was inhibited in LY294002 group, (P <0.05), and the expression of LY294002 + in irradiation group was lower than that in irradiation group (P <0.05). The proportion of cells in G2 phase in LY294002 group was significantly lower than that in control group (P <0.01), and the proportion of cells in G2 phase of LY294002 + irradiation group was significantly lower than that of irradiation group (P <0.05) .Conclusion: LY294002 PI3K inhibitor has a significant effect on Eca-109 cells Sensitization, the mechanism may inhibit tumors Cellular DNA double strand break repair genes and DNA-PKcs reduce G2 cell arrest.