朱孝峰, 周军民, 谢冰芬, 冯公侃, 刘宗潮, 曾益新. HER2/neu受体酪氨酸激酶抑制剂SUCI02对乳腺癌细胞周期的影响及其分子机理[J]. 中国肿瘤临床, 2004, 31(22): 1261-1264.
引用本文: 朱孝峰, 周军民, 谢冰芬, 冯公侃, 刘宗潮, 曾益新. HER2/neu受体酪氨酸激酶抑制剂SUCI02对乳腺癌细胞周期的影响及其分子机理[J]. 中国肿瘤临床, 2004, 31(22): 1261-1264.
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Zhu Xiaofeng, Zhou Junmin, Xie Bingfen, Feng Gongpei, Liu Zongchao, Zeng Yixin. HER2/neu Tyrosine Kinase Inhibitor SUCI02 Induces Cell Cycle Arrest in HER2/neu-overexpressing Breast Cancer Cells and Its Mechanism[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2004, 31(22): 1261-1264.
Citation: Zhu Xiaofeng, Zhou Junmin, Xie Bingfen, Feng Gongpei, Liu Zongchao, Zeng Yixin. HER2/neu Tyrosine Kinase Inhibitor SUCI02 Induces Cell Cycle Arrest in HER2/neu-overexpressing Breast Cancer Cells and Its Mechanism[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2004, 31(22): 1261-1264.
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HER2/neu受体酪氨酸激酶抑制剂SUCI02对乳腺癌细胞周期的影响及其分子机理

HER2/neu Tyrosine Kinase Inhibitor SUCI02 Induces Cell Cycle Arrest in HER2/neu-overexpressing Breast Cancer Cells and Its Mechanism

    摘要
  • 摘要: 目的 :探讨SUCI02对HER2受体过表达的乳腺癌细胞周期分布的影响及其分子机制。 方法 :采用免疫印迹法检测蛋白表达量和磷酸化蛋白量的变化;流式细胞术检测细胞周期的分布。RT-PCR检测mRNA的表达。 结果 :SUCI02处理MDA-MB-453细胞24h后,流式细胞仪分析可见在0、2.5、5、10、20μg/ml浓度下,MDA-MB-453细胞G0/G1期分别为:59.5%、65.8%、68.2%、70.0%、79.0%;S期分别为:38.1%、31.9%、29.4%、27.4%、18.3%;G2M期分别为:2.4%、2.3%、2.4%、2.6%、2.7%。不同浓度的SUCI02处理MDA-MB-453细胞24h后,细胞中p27上调,Rb的高磷酸化状态下降,CyclinD1蛋白水平在10、20μg/mlSUCI02作用下显著下降。RT-PCR检测结果可见SUCI02对CyclinD1的mRNA表达有明显的抑制作用。 结论 :SUCI02能诱导HER2/neu过表达的乳腺癌MDA-MB-453细胞停止于G1期,且与p27上调、Rb的高磷酸化状态下降、CyclinD1mRNA和蛋白水平下降有关。

     

    Abstract: Objective :To observe the effect of SUCI02 on cell cycle in HER2/neu-overexpress-ing MDA-MB-453 cells and its mechanism. Methods :The cell cycle distribution was examined using flow cytometry. The protein expression was detected with immunoblot analysis. The levels of mRNA was detected by RT-PCR method. Results :Under concentrations of 0, 1.25, 2.5, 5.0, 10 and 20!g/ml, the percentages of G0/Gi in MDA-MB-453 were 59.5X, 65.8%, 68.2%, 70.0X and 79.0X ； the percentages of S phase were 38.1%, 31.9%, 29.4%, 27.4% and 18.3%; the percentages of G2M phase were 2.4%, 2.3% 2.4%, 2.6%, 2.7%, respectively. After MDA-MB-453 cells were treated with different concentrations of SUCI02 for 24h, immunoblot assay showed up -regulation of p27 protein expression and decrease of hyperphosphorylated Rb and cyclin D1 protein expression. The levels of Cyclin D1 mRNA decreased following SUCI02 treatment. Conclusions :SUCI02 induces G1 arrest in HER2/neu-overex-pressing MDA-MB-453 cancer cells. G1 arrest is associated with p27 up -regulation, decrease of cy-clinD1 protein and cyclinD 1 mRNA and hyperphosphorylated R.

     

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