摘要
目的:研究塞来昔布增强胃癌BGC823细胞对雷帕霉素的敏感性,探讨PI3K/Akt信号通路在塞来昔布增强胃癌BGC823细胞对雷帕霉素敏感性中的作用。方法:MTT法检测细胞对药物敏感性。Western blot法检测Akt和p-Akt蛋白表达。结果:100nmol/L雷帕霉素作用于BGC823胃癌细胞72h后,细胞存活抑制率不足30%。雷帕霉素可活化PI3K/Akt通路,PI3K抑制剂LY294002(25μmol/L)预处理细胞1h后再予雷帕霉素作用72h,与单药雷帕霉素组相比,细胞存活率明显降低[(54.2±1.4)%和(83.6±2.3)%,P<0.05]。塞来昔布(40μmol/L)可明显抑制雷帕霉素引起的p-Akt活化,进而增强胃癌BGC823细胞对雷帕霉素的敏感性,细胞存活率从(81.9±2.3)%降至(51.5±4.4)%(P<0.05)。结论:塞来昔布通过抑制雷帕霉素诱导的PI3K/Akt活化,增强胃癌BGC823细胞对雷帕霉素的敏感性。
Objective： To investigate the effect of celecoxib combined with rapamycin on the survival of BGC823 cells and the role of phosphoinositide 3-kinases（ PI3K） / Akt signaling pathway in celecoxib sensitization to rapamycin. Methods： Cell proliferation was measured using MTT assay. The expression of Akt and phosphor-Akt was derermined by Western blotting. Results： The level of growth inhibition was less than 30% in BGC823 cells after exposure to rapamycin（ 100 nmol / L） for 72 h. Rapamycin induced Akt activation. Pretreated with PI3 K inhibitor LY294002（ 25μmol/L） for 1h followed by exposure to rapamycin for 72 h,the level of cell viability was obviously lower [（ 54. 2± 1. 4） % and（ 83. 6 ± 2. 3） %,P〈0. 05] than the rapamycin only. Treatment with 40μmol / L celecoxib repressed the activation of PI3 K / Akt signaling,and enhanced the sensitivity of cells to rapamycin,the rate of cell viability decreased to（ 51. 5 ± 4. 4） %（ P〈0. 05）. Conclusion： Celecoxib sensitized gastric cancer BGC823 cells to rapamycin by inhibiting rapamycin induced the activaton of PI3 K / Akt signaling.
出处
《现代肿瘤医学》
CAS
2016年第4期509-512,共4页
Journal of Modern Oncology
基金
国家自然科学基金(编号:81172369
81372547)
