期刊文献+

异甘草素通过PI3K/Akt通路诱导人胃癌SGC7901细胞凋亡

Isoliquiritigenin induces apoptosis of human gastric carcinoma SGC7901 cells through PI3K/AKT pathway
下载PDF
导出
摘要 目的:初步研究异甘草素(isoliquiritigenin ISL)对人胃癌SGC7901细胞凋亡诱导作用的影响,并探讨信号通路中蛋白质丝氨酸苏氨酸激酶(protein kinase B,Akt)、磷酸化Akt(PAkt)及下游凋亡蛋白Bax表达水平的变化.方法:取对数生长期人胃癌SGC7901细胞分为对照组、ISL实验组,培养24、48、72 h后采用MTT实验检测ISL对细胞生长的抑制情况,摸索后续实验药物浓度和作用时间;应用流式细胞仪检测各组细胞凋亡情况;应用Western blot法检测凋亡调节蛋白Bax、Ak和P-Akt的表达.结果:10mmol/L ISL不能抑制胃癌细胞株SGC7901的生长,而25、50、100mm o l/LISL可明显抑制其生长,且呈时间和浓度依赖性.与对照组凋亡率3.23%±0.45%相比,25mmol/L组(6.13%±0.61%)、50mmol/L组(11.70%±0.75%)、100mmol/L组(26.60%±1.51%)凋亡率逐渐增高(P<0.05)随ISL浓度的增加,P-Akt蛋白表达水平逐渐降低,凋亡蛋白Bax表达水平逐渐增加(均P<0.05),各组间A k t蛋白水平差异无统计学意义.结论:ISL能够诱导SGC7901细胞凋亡,其机制可能与下调PI3K/AKT信号转导通路蛋白的表达以及上调其下游的凋亡蛋白Bax有关. AIM:To investigate the effect of isoliquiritigenin(ISL) on the apoptosis of human gastric carcinoma SGC7901 cells and to explore the possible mechanism involved.METHODS:SGC7901 cells in logarithmic growth phase were divided into a control group and an ISL group.After cells were treated with different concentrations of ISL for different durations,cell proliferation was assessed by MTT assay,apoptosis of SGC7901 cells was assessed by flow cytometry,and the expression of Bax,Akt,and P-Akt was tested by Western blot.RESULTS:The proliferation of SGC7901 cells could not be inhibited by 10 μmol/L ISL,but was significantly inhibited by 25 μmol/L,50 μmol/L,and 100 μmol/L ISL,and the inhibitory effect was concentration- and timedependent.Compared with the control group(3.23%± 0.45%),the apoptosis rates of cells treated with 25 μmol/L(6.13%± 0.61%),50μmol/L(11.70%± 0.75%),and 100 μnol/L ISL(26.60%± 1.51%) significantly increased(P〈0.05).The expression level of P-Akt decreased gradually and Bax increased gradually with the increase of the ISL concentration(P〈0.05).There was no statistically significant difference between groups in the expression level of Akt protein.CONCLUSION:ISL can significantly induce the apoptosis of SGC7901 cells,possibly via mechanisms related to downregulation of the expression of signal transduction pathways protein PI3K/AKT and upregulation of its downstream protein Bax.
出处 《世界华人消化杂志》 CAS 2015年第33期5342-5347,共6页 World Chinese Journal of Digestology
关键词 异甘草素 胃癌 凋亡 Bax 磷脂酰肌醇3-激酶/蛋白质丝氨酸苏氨酸激酶 磷酸化蛋白激酶B Isoliquiritigenin Gastric carcinoma Apoptosis Bax Phosphatidylinositol 3 kinase/ protein kinase B P-Akt
  • 相关文献

参考文献4

二级参考文献152

  • 1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
  • 2张晶,杨静,汤宏斌.异甘草素对人宫颈癌细胞增殖的抑制作用[J].中国药理学与毒理学杂志,2005,19(6):436-442. 被引量:17
  • 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
  • 4Huang S, Houghton PJ. Targeting mTOR signaling for cancer therapy[J]. Curt Opin Pharmacol,2003,3(4) :371-377.
  • 5Gao N,Flynn DC,Zhang Z,et al. G1 cell cycle progressian and the expression of G1 cyclins are regulated by PI3K/AKT/mTOR/ p70S6K1 signaling in human ovarian cancer cells[J]. Am J Physiol Cell Physiol,2004,287(2) :C281-291.
  • 6Hofseth LJ, Hussain SP, Wogan GN, et al. Nitric oxide in cancer and chemoprevention [ J ]. Free Radic B iol Med,2003,34 (8) :955- 968.
  • 7Hill MM ,Hemmings BA. Inhibition of protein kinase B/Akt. implications for cancer therapy [ J ]. Pharmacol Ther, 2002,93 ( 2/3 ) : 243 -251.
  • 8Qian Y, Corum L, Meng Q, et al. PI3 K induced actin filament remodeling through Akt and pTOS6K1 :implication of essential role in cell migration [ J ]. Am J Physiol Cell Physio ,2004,286 (1) :C153- C163.
  • 9Kim D, Kim S, Koh H, et al. Akt/PKB promotes cancer cell invasion via increased motility and metalloproteinase production [ J ]. FASE J,2001,15 ( 11 ) : 1953-1962.
  • 10Grille SJ, Bellacosa A, Upson J, et al. The protein kinase Akt induces epithelial mesenchymal transition and promotes enhanced motility and invasiveness of squamous cell carcinoma lines [ J ]. Cancer Res,2003,63 (9) :2172-2178.

共引文献152

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