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LY294002对人胃癌HGC-27细胞增殖的影响 被引量:1

Effect of LY294002 on the proliferation of gastric carcinoma cell HGC-27
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摘要 目的探讨PI3K特异性抑制剂LY294002对胃癌HGC-27细胞增殖的影响。方法用不同浓度(0、10、20、40μmol.L-1)的LY294002对细胞进行干预至不同的时间(20、40、60 h),CCK-8法检测细胞增殖,流式细胞仪(PI染色)检测细胞周期。结果 LY294002作用于HGC-27细胞后,不同浓度的LY294002均对人胃癌HGC-27细胞具有明显的抑制生长作用,并随着剂量的增加而逐渐增强(P=0.000);当LY294002浓度为40μmol.L-1时,LY294002对HGC-27细胞的抑制作用随着培养时间的延长而逐渐增强(P=0.000)。细胞周期分析显示LY294002作用60 h后,呈浓度依赖性改变细胞周期的分布,G0/G1期细胞比例逐渐上升,S期细胞比例逐渐下降,G2/M期细胞比例逐渐增加,细胞周期发生G0/G1期、G2/M期阻滞。结论 LY294002作用于HGC-27细胞后,能够抑制细胞增殖和细胞周期的进展。 Aim To investigate the effects of the specific PI3K inhibitor LY294002 on the proliferation in gastric carcinoma HGC-27.Methods The HGC-27 cells were incubated with different concentrations(0,10,20 and 40 μmol·L-1 separately) of LY294002 for different times(20,40 and 60 h separately).CCK-8 was taken to test the cell proliferation.Propidium Iodide dying was taken to test the dislocation of cell cycle.Results After the HGC-27 cells were treated with LY294002,the cell proliferation was inhibited,and the effect of proliferation inhibition was increased with the concentrions(P=0.000).The effect of proliferation inhibition was increased with interfering times when the concentrions of LY294002 was 40 μmol·L-1(P=0.000).The cell cycle analysis showed the dose-dependent manner,the rate of G0/G1 and G2/M stage cells was increased,and the rate of S stage cells was decreased with concentrions when the interfering time was 60 h(P=0.000).Conclusion LY294002 can inhibit the proliferation and the cell cycle progression of HGC-27 cells.
出处 《安徽医药》 CAS 2011年第2期192-194,共3页 Anhui Medical and Pharmaceutical Journal
关键词 PI3K抑制剂 胃癌细胞 细胞增殖 细胞周期 PI3K inhibitor helicobacter pylor cell proliferation cell cycle
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  • 1赵灵芝,银巍,苏兴文,肖茹,曹林,邱鹏新,颜光美.IGF-1经PI3K/Akt依赖性途径保护苯妥英诱导的小脑颗粒神经元凋亡[J].中国药理学通报,2005,21(1):53-57. 被引量:14
  • 2夏曙,于世英.抑制PI3K/Akt信号转导通路提高化疗效果的实验研究[J].肿瘤,2006,26(4):311-313. 被引量:21
  • 3王玲,刘世坤,周于禄,裴奇.华蟾素对人乳腺癌细胞阿霉素多药耐药性的逆转作用[J].中国药理学通报,2007,23(5):677-680. 被引量:38
  • 4Han Z, Hong L, Han Y, et al. Phospho Akt mediates muhidrug resistance of gastric cancer ceils through regulation of P-gp, Bcl-2 and Bax[ J]. J Exp Clin Cancer Res,2007,26( 2 ) :261 -8.
  • 5Misra S,Ghatak S,Toole B P. Regulation of MDR1 expression and drug resistance by a positive feedback loop involving hyaluronan, phosphoinositide 3-kinase, and ErbB2 [ J ]. J Biol Chem,2005 ,280 (21) :20310 - 5.
  • 6Michl P, Downward J. Mechanisms of disease:PI3 K/AKT signaling in gastrointestinal cancers [ J ]. J Gastroenterol, 2005,43 ( 10 ) : 1133 -9.
  • 7Nam S Y, Lee H S, Jung G A, et al. Akt/PKB activation in gastric carcinomas correlates with clinicopathologic variables and prognosis [J]. APMIS,2003 ,111(12) :1105 - 13.
  • 8Ghosh S, Karln M. Missing pieces in the NF-kappaB puzzle [ J ]. Cell,2002,109Suppl: S81 - 96.
  • 9Zhang D, Fan D. Multidrug resistance in gastric cancer: recent research advances and ongoing therapeutic challenges [ J ]. Exp Rev Anticancer Ther,2007,7 (10) : 1369 - 78.
  • 10Ambudkar, Suresh V, Kimchi-Sarfaty C, et al. P-glycoprotein: from genomics to mechanism [ J ]. Oncogene, 2003,22 ( 47 ) : 7468 - 85.

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