...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cancer science. >SUCI02 inhibits the erbB-2 tyrosine kinase receptor signaling pathway and arrests the cell cycle in G1 phase in breast cancer cells.
【24h】

SUCI02 inhibits the erbB-2 tyrosine kinase receptor signaling pathway and arrests the cell cycle in G1 phase in breast cancer cells.

机译：SUCI02抑制erbB-2酪氨酸激酶受体信号传导途径，并阻止乳腺癌细胞G1期的细胞周期。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The erbB-2 gene encodes tyrosine kinase receptor p185(neu). Overexpression of erbB-2 plays a key role in tumorigenesis and the progression of tumors such as breast cancer and ovarian cancer. Our investigation suggests that the anti-inflammatory agent N-(4-ethoxyphenol)-2-hydroxy-acid amide (SUCI02) reversibly represses tyrosine phosphorylation of erbB-2 in a dose-dependent manner, with half maximal inhibition occurring at a concentration of 21.05 micromol/L without reduced erbB-2 receptor expression. Activation of mitogen-activated protein kinase and protein kinase B, downstream molecules of the erbB-2-mediated signal transduction pathway, was inhibited following exposure to SUCI02. In contrast, tyrosine phosphorylation of epidermal growth factor receptor (EGFR) was relatively unaffected by SUCI02. Proliferation of erbB-2-overexpressing BT474 cells was inhibited to a greater extent than proliferation of EGFR-overexpressing A431 cells following exposure to SUCI02. SUCI02 induced cell cycle arrest in G(1) phase with upregulation of p27 and downregulation of pRb phosphorylation. Systemic administration of SUCI02 in nude mice resulted in inhibition of erbB-2 tyrosine kinase phosphorylation of subcutaneous human breast cancer BT474 xenografts. We conclude that SUCI02 inhibits erbB-2 tyrosine kinase phosphorylation in vitro and in vivo, shuts down the erbB-2 downstream pathway and induces cell cycle arrest in G(1) phase. These results suggest that SUCI02 is a potential novel anticancer agent that deserves further investigation. (Cancer Sci 2006; 97: 84-89).
机译：erbB-2基因编码酪氨酸激酶受体p185（neu）。 erbB-2的过表达在肿瘤发生和诸如乳腺癌和卵巢癌的肿瘤进展中起关键作用。我们的研究表明，抗炎药N-（4-乙氧基苯酚）-2-羟基酸酰胺（SUCI02）以剂量依赖的方式可逆地抑制erbB-2的酪氨酸磷酸化，当浓度为时，抑制作用最大一半。不降低erbB-2受体表达的21.05微摩尔/升。暴露于SUCI02后，抑制了erbB-2介导的信号转导途径下游分子丝裂原活化的蛋白激酶和蛋白激酶B的活化。相反，表皮生长因子受体（EGFR）的酪氨酸磷酸化相对不受SUCI02的影响。暴露于SUCI02后，表达erbB-2的BT474细胞的增殖比表达EGFR过高的A431细胞的增殖受到更大程度的抑制。 SUCI02诱导细胞周期停滞在G（1）期，p27上调，pRb磷酸化下调。在裸鼠中全身施用SUCI02可抑制皮下人乳腺癌BT474异种移植物的erbB-2酪氨酸激酶磷酸化。我们得出的结论是，SUCI02在体外和体内抑制erbB-2酪氨酸激酶磷酸化，关闭erbB-2下游途径并诱导G（1）期细胞周期停滞。这些结果表明，SUCI02是潜在的新型抗癌剂，值得进一步研究。 （Cancer Sci 2006; 97：84-89）。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号