...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular Carcinogenesis >Role of mitogen-activated protein kinases in phenethyl isothiocyanate-induced apoptosis in human prostate cancer cells.
【24h】

Role of mitogen-activated protein kinases in phenethyl isothiocyanate-induced apoptosis in human prostate cancer cells.

机译：丝裂原活化蛋白激酶在苯硫异氰酸酯诱导的人前列腺癌细胞凋亡中的作用。

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 present study was undertaken to examine the role of mitogen-activated protein kinases (MAPKs) in apoptosis induction by phenethyl isothiocyanate (PEITC), a cruciferous vegetable-derived cancer chemopreventive agent, with DU145 and LNCaP human prostate cancer cells as a model. The MAPK family of serine/threonine kinases, including extracellular signal-regulated kinase1/2 (ERK1/2), c-jun N-terminal kinase1/2/3 (JNK1/2/3), and p38 MAPK play an important role in cell proliferation and apoptosis in response to different stimuli. Exposure of DU145 and LNCaP cells to growth suppressive concentrations of PEITC resulted in activation of ERK1/2 and JNKs, but not p38 MAPK, in both cell lines. In DU145 cells, the apoptosis induction by PEITC was statistically significantly attenuated by pharmacological inhibition of JNKs with SP600125. Adenovirus-mediated overexpression of Flag-tagged JNK binding domain (JBD) of JNK-interacting protein-1 (JIP-1), an inhibitor of JNK, also inhibited PEITC-induced apoptosis in DU145 cells. On the other hand, inhibition of ERK1/2 activation with MEK1 inhibitor PD98059 failed to offer protection against PEITC-induced apoptosis in DU145 cells. In LNCaP cells, the PEITC-induced cell death was not affected by either pretreatment with PD98059 or SP600125 or overexpression of JBD of JIP-1. These results indicate that involvement of MAPKs in apoptosis induction by PEITC in human prostate cancer cells is cell line-specific.
机译：本研究以DU145和LNCaP人前列腺癌细胞为模型，研究了丝裂素活化的蛋白激酶（MAPK）在十字花科植物性癌症化学预防剂苯乙基异硫氰酸酯（PEITC）诱导凋亡中的作用。 MAPK家族的丝氨酸/苏氨酸激酶，包括细胞外信号调节激酶1/2（ERK1 / 2），c-jun N-末端激酶1/2/3（JNK1 / 2/3）和p38 MAPK在其中起重要作用细胞增殖和凋亡对不同刺激的反应。将DU145和LNCaP细胞暴露于PEITC的生长抑制浓度下，导致两种细胞系中ERK1 / 2和JNKs激活，但未激活p38 MAPK。在DU145细胞中，PEITC对细胞凋亡的诱导在统计学上被SP600125对JNKs的药理抑制显着减弱。腺病毒介导的JNK相互作用蛋白1（JIP-1）的Flag标记JNK结合域（JBD）的过表达，JNK的抑制剂，也抑制了PEITC诱导的DU145细胞凋亡。另一方面，用MEK1抑制剂PD98059抑制ERK1 / 2活化不能提供针对PEITC诱导的DU145细胞凋亡的保护作用。在LNCaP细胞中，PEITC诱导的细胞死亡不受PD98059或SP600125的预处理或JIP-1的JBD过表达的影响。这些结果表明，MAPK参与人前列腺癌细胞的PEITC诱导的凋亡是细胞系特异性的。

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