• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of Nutritional Biochemistry >Isoliquiritigenin inhibits migration and invasion of prostate cancer cells: possible mediation by decreased JNK/AP-1 signaling
【24h】

Isoliquiritigenin inhibits migration and invasion of prostate cancer cells: possible mediation by decreased JNK/AP-1 signaling

机译：异quiritigeninin抑制前列腺癌细胞的迁移和侵袭：可能通过降低JNK / AP-1信号传导来介导

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

Isoliquiritigenin (ISL, 4,2',4'-trihydroxychalcone), which is found in licorice, shallot and bean sprouts, is a potent antioxidant with anti-inflammatory and anti-carcinogenic effects. The purpose of this study was to investigate the effects of ISL treatment on the migration, invasion and adhesion characteristics of DU145 human prostate cancer cells. DU145 cells were cultured in the presence of 0-20 omol/L ISL with or without 10 og/L epidermal growth factor (EGF). ISL inhibited basal and EGF-induced cell migration, invasion and adhesion dose dependently. ISL decreased EGF-induced secretion of urokinase-type plasminogen activator (uPA), matrix metalloproteinase (MMP)-9, tissue inhibitor of metalloproteinase-1 (TIMP-1), and vascular endothelial growth factor (VEGF), but increased TIMP-2 secretion in a concentration-dependent manner. In addition, ISL decreased the protein levels of integrin-l2, intercellular adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM), and mRNA levels of uPA, MMP-9, VEGF, ICAM and integrin-l2. Furthermore, basal and EGF-induced activator protein (AP)-1 binding activity and phosphorylation of Jun N-terminal kinase (JNK), c-Jun and Akt were decreased after ISL treatment. However, phosphorylation of extracellular signal-regulated kinase (ERK)1/2 and p38 mitogen-activated protein kinase was not altered. The JNK inhibitor SP600125 inhibited basal and EGF-induced secretion of uPA, VEGF, MMP-9 and TIMP-1, as well as AP-1 DNA binding activity and cell migration. These results provide evidence for the role of ISL as a potent antimetastatic agent, which can markedly inhibit the metastatic and invasive capacity of prostate cancer cells. The inhibition of JNK/AP-1 signaling may be one of the mechanisms by which ISL inhibits cancer cell invasion and migration.
机译：异甘草酸生成素（ISL，4,2'，4'-三羟基查尔酮）存在于甘草，青葱和豆芽中，是一种有效的抗氧化剂，具有抗炎和抗癌作用。这项研究的目的是调查ISL处理对DU145人前列腺癌细胞的迁移，侵袭和粘附特性的影响。 DU145细胞在有或没有10 og / L表皮生长因子（EGF）的0-20 omol / L ISL存在下培养。 ISL依赖性地抑制基础和EGF诱导的细胞迁移，侵袭和粘附剂量。 ISL降低了EGF诱导的尿激酶型纤溶酶原激活物（uPA），基质金属蛋白酶（MMP）-9，金属蛋白酶-1（TIMP-1）和血管内皮生长因子（VEGF）的分泌，但增加了TIMP-2以浓度依赖性方式分泌。此外，ISL降低了整联蛋白-12，细胞间粘附分子（ICAM）和血管细胞粘附分子（VCAM）的蛋白质水平，以及uPA，MMP-9，VEGF，ICAM和整联蛋白-12的mRNA水平。此外，ISL处理后，基础和EGF诱导的激活蛋白（AP）-1结合活性和Jun N末端激酶（JNK），c-Jun和Akt的磷酸化降低。但是，细胞外信号调节激酶（ERK）1/2和p38丝裂原活化蛋白激酶的磷酸化没有改变。 JNK抑制剂SP600125抑制基础和EGF诱导的uPA，VEGF，MMP-9和TIMP-1的分泌，以及AP-1 DNA结合活性和细胞迁移。这些结果提供了ISL作为有效抗癌剂的作用的证据，它可以显着抑制前列腺癌细胞的转移和侵袭能力。 JNK / AP-1信号的抑制可能是ISL抑制癌细胞入侵和迁移的机制之一。

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