基础医学与临床 ›› 2013, Vol. 33 ›› Issue (5): 609-613.

• 研究论文 • 上一篇    下一篇

吉妥辛对吉非替尼耐药性非小细胞肺癌的抑制作用

薛毅博1,郑直2   

  1. 1. 中国医学科学院基础医学研究所&北京协和医学院基础学院
    2. 中国医学科学院基础医学研究所
  • 收稿日期:2013-01-31 修回日期:2013-03-19 出版日期:2013-05-05 发布日期:2013-05-29
  • 通讯作者: 郑直 E-mail:zhizheng10@yahoo.com

Inhibitory effect of gitoxin on non-small cell lung cancer with gefitinib resistance

  • Received:2013-01-31 Revised:2013-03-19 Online:2013-05-05 Published:2013-05-29

摘要: 目的 在细胞和动物水平评价强心苷药物吉妥辛对耐药性非小细胞肺癌的抑制作用,并对其抑癌的分子机制进行初步探索。方法 吉妥辛和吉非替尼处理H1975细胞后,用MTS法检测细胞的存活率,流式细胞分析法检测细胞的凋亡率;吉妥辛处理移植瘤裸鼠,测量并计算移植瘤体积;吉妥辛处理H1975细胞后,用Western blot检测Erk1/2的磷酸化水平。结果 吉妥辛比吉非替尼更有效地抑制H1975的生长(P<0.05),促进其凋亡(P<0.05),且能显著抑制裸鼠移植瘤的生长(P<0.05)。吉妥辛能计量和时间依赖地抑制Erk1/2的磷酸化(P<0.05)。结论 吉妥辛可作为治疗耐药性非小细胞肺癌的潜在替代药物。

关键词: 吉妥辛, H1975, 小鼠肿瘤模型, Erk1/2信号通路

Abstract: Objective To evaluate the inhibitory effect of gitoxin on non small cell lung cancer with drug-resistance in vitro and in vivo and explore the underlying molecular mechanism Methods Survival and apoptosis rates of H1975 were measured by MTS assay and flow cytometry respectively after gitoxin and gefitinib treatments. Tumor volumes of gitoxin treated xenograft nude mice were calculated by measuring the lengths and widths of these tumors. The phosphorylation of Erk1/2 was analyzed by Western blot. Results Gitoxin can inhibit the growth of H1975 and induce its apoptosis more effectively than gefitinib. It can also inhibit growth of transplanted tumors in nude mice. In addition, gitoxin can inhibit the phosphorylation of Erk1/2 in a dosage and time-point dependent way. Conclusion Gitoxin may offer a potential treatment for drug resistant NSCLC.

Key words: gitoxin, H1975, xenograft nude mouse model, Erk1/2 signal pathway

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