郑青, 彭菲, 吴晓萍, 苏志坚, 李校堃. nmhaFGF对人乳腺癌细胞增殖的影响及相关机制J. 药学学报, 2006, 41(3): 263-267.
引用本文: 郑青, 彭菲, 吴晓萍, 苏志坚, 李校堃. nmhaFGF对人乳腺癌细胞增殖的影响及相关机制J. 药学学报, 2006, 41(3): 263-267.
ZHENG Qing, PENG Fei, WU Xiao-ping, SU Zhi-jian, LI Xiao-kun. Effect and mechanism of action of non-mitogenetic human acidic fibroblast growth factor on the mitogenic activity of the mammary tumor cellJ. Acta Pharmaceutica Sinica, 2006, 41(3): 263-267.
Citation: ZHENG Qing, PENG Fei, WU Xiao-ping, SU Zhi-jian, LI Xiao-kun. Effect and mechanism of action of non-mitogenetic human acidic fibroblast growth factor on the mitogenic activity of the mammary tumor cellJ. Acta Pharmaceutica Sinica, 2006, 41(3): 263-267.

nmhaFGF对人乳腺癌细胞增殖的影响及相关机制

Effect and mechanism of action of non-mitogenetic human acidic fibroblast growth factor on the mitogenic activity of the mammary tumor cell

  • 摘要: 目的比较nmhaFGF和haFGF对恶性肿瘤细胞的促增殖作用及其机制,探讨nmhaFGF临床应用的安全性。方法以haFGF和nmhaFGF分别处理人乳腺癌细胞(MCF-7),用MTT法检测其细胞增殖活性;用流式细胞技术分析细胞周期;用蛋白免疫印迹法半定量检测MAPK通路中的信号蛋白Grb2和ERK1/2在MCF-7中的表达。结果nmhaFGF对MCF-7细胞的促增殖作用明显低于haFGF;haFGF组G1/G0和G2/M期细胞比例均低于nmhaFGF组和对照组,S期细胞比例显著高于nmhaFGF组和对照组;nmhaFGF组的Grb2和ERK1/2信号蛋白表达水平均低于haFGF组,亦接近对照组。结论nmhaFGF的促增殖活性显著下降,其机制是通过下调MAPK信号通路中的Grb2和ERK1/2信号分子的表达来实现的。

     

    Abstract: AimTo compare the effects of the non-mitogenetic human acidic fibroblast growth factor (nmhaFGF) and the human acidic fibroblast growth factor (haFGF) on the proliferation and MAPK signal transduction pathway of the malignant tumor cell and to study the clinical safety of nmhaFGF. Methods The mammary tumor cells (MCF-7) were treated with haFGF and nmhaFGF separately. The mitogenic activities of both haFGF and nmhaFGF were detected by MTT method and the cell cycle was analyzed by flow cytometer (FCM). The expression levels of the signal proteins, Grb2 (growth factor receptor bound 2) and ERK1/2 (extracellular signal-regulated kinase 1/2), were detected by semi-quantitative Western blotting method. ResultsThe mitogenic activity of nmhaFGF was obviously lower than that of haFGF. The activity of nmhaFGF was weaker than that of the haFGF. The ratio of G1/G0, G2/M of haFGF was markedly lower than that of nmhaFGF and control group, and was reverse in S phase. The expression levels of both Grb2 and ERK1/2 of the nmhaFGF treated group were lower than that of the haFGF treated group and approaching the control group. ConclusionThe mitogenic activity of the nmhaFGF decreased remarkably. Its mechanism probably via down-regulation of the expression of the signal moleculars, MAPK-ERK1/2 and Grb2.

     

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