期刊文献+

姜黄素对HL60细胞PI3K/AKT信号传导通路的影响 被引量:3

Effects of curcumin on PI3K/AKT signaling pathway in HL60 Cells
下载PDF
导出
摘要 目的研究姜黄素诱导白血病HL-60细胞凋亡与PI3K/AKT信号传导通路的相关性,为AML的靶向治疗提供新思路。方法 MTT实验检测姜黄素对HL-60细胞增殖的抑制作用;经姜黄素处理后,用倒置显微镜进行细胞形态学观察,并用Western blot检测CAV-1、AKT、p-AKT蛋白水平。结果 MTT实验证明了姜黄素对HL60细胞增殖具有抑制作用,且随作用浓度的增强而增强;姜黄素作用HL-60细胞,用倒置显微镜观察细胞出现了凋亡形态学改变;并且Western blot检测显示CAV-1蛋白水平增高,而AKT、p-AKT蛋白水平降低。结论姜黄素可通过上调HL-60细胞中CAV-1的表达,而抑制PI3K/AKT信号通路,进而抑制HL-60细胞增殖并促进其凋亡。 Objective To investigate the effects of curcumin on the PI3K/AKT signaling pathway in HL60 cells and the apoptosis of ilL60 cells. Methods The inhibitory effects of curcumin on the proliferation of ilL60 ceils were determined by MTT assay. After being treated by curcumin, the morphological and structural changes of the cells were observed by inverted microscope. The levels of CAV-1, AKT and p-AKT protein were measured by Western blotl Results MTT assay revealed that curcumin has growth-inhibiting effects on I-IL60 cells, and the effects were en- haneed with the increase of concentration. Apoptotic morphology changes were observed by inverted microscope. The level of CAV-1 protein was increased, while the levels of AKT and p-AKT protein were reduced. Conclusion Curcumin can inhibit PI3K/AKT signaling pathway by upregulating the expression of CAV-1, resulting in inhibiting cell proliferation and promoting apoptosis in HL60 cells.
作者 闵旻 高清平
出处 《海南医学》 CAS 2012年第6期3-5,共3页 Hainan Medical Journal
关键词 姜黄素 HL-60 PI3K AKT P-AKT Curcumin I-IL-60 PI3K AKT p-A
  • 相关文献

参考文献3

二级参考文献59

  • 1Hui-QingJiang,Xiao-LanZhang,LiLiu,Chang-ChunYang.Relationship between focal adhesion kinase and hepatic stellate cell proliferation during rat hepatic fibrogenesis[J].World Journal of Gastroenterology,2004,10(20):3001-3005. 被引量:19
  • 2康春生,浦佩玉,李捷,王广秀.反义及显性负调节AKT2 RNA对脑胶质瘤细胞增殖抑制作用的体外研究[J].癌症,2004,23(11):1267-1272. 被引量:5
  • 3王宏梅,陈龙华,郑小康,李启生,伍新尧,夏云飞.抑制ATM/PI3K功能区表达对鼻咽癌细胞CNE1辐射增敏的研究[J].癌症,2006,25(9):1097-1101. 被引量:9
  • 4Atkins M B, Hidalgo M, Stadler W M, et al. Randomized phase Ⅱ study of multiple dose levels of CCI-779, a novel mammalian target of rapamycin kinase inhibitor, in patients with advanced refractory renal cell carcinoma [J]. J Clin Oncol, 2004, 22(5) :909-918.
  • 5Christian T, James R, Zoran F, et al. Small-molecule MDM2 antagonists reveal aberrant p53 signaling in cancer : implications for therapy [ J ]. Proc Natl Acad Sci USA, 2006,103 (6) : 1888-1893.
  • 6Adachi S, Leoni L M, Carson D A, et al. Apoptosis induced by molecular targeting therapy in hematological malignancies [J]. Acta Haematol, 2004,111(1-2) : 107-123.
  • 7Campiglio M, Olgiati C, Normanno N, et al. Inhibition of proliferation and induction of apoptosis in breast cancer cells by the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor ZD1839 ( 'Iressa' ) is independent of EGFR expression level [J]. J Cell Physiol, 2004,198(2): 259-268.
  • 8Zhang M, Fang X, Liu H, et al. Blockade of AKT activation in prostate cancer cells with a small molecule inhibitor, 9-chIoro-2-methylellipticinium acetate (CMEP) [J]. Biochem Pharmacol, 2007,73( 1 ) : 15-24.
  • 9Douglas A L, Faina B, Cindy J Y, et al. Frequent mutation of the P1K3CA gene in ovarian and breast cancer [J]. Clin Cancer Res, 2005,11 (8):2875- 2878.
  • 10Knobbe C B, Kieslich A T, Reifenberger G. Genetic alteration and expression of the phosphoinositol-3- kinase/Akt pathway genes P1K3CA and PIKE in human glioblastomas [J]. Neuropathol Appl Neurobiol, 2005, 31 (5) :486-490.

共引文献139

同被引文献41

引证文献3

二级引证文献39

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部