...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of applied toxicology >Downregulation of human colon carcinoma cell (COLO-205) proliferation through PKG-MAP kinase mediated signaling cascade by E. coli heat stable enterotoxin (STa), a potent anti-angiogenic and anti-metastatic molecule.
【24h】

Downregulation of human colon carcinoma cell (COLO-205) proliferation through PKG-MAP kinase mediated signaling cascade by E. coli heat stable enterotoxin (STa), a potent anti-angiogenic and anti-metastatic molecule.

机译：通过大肠杆菌热稳定肠毒素（STa）（一种有效的抗血管生成和抗转移分子），通过PKG-MAP激酶介导的信号级联反应下调人结肠癌细胞（COLO-205）的增殖。

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

It was reported earlier that Escherichia coli heat stable enterotoxin (STa), a major causative agent of secretory diarrhea, can also inhibit the proliferation of colon carcinoma cells with the involvement of cGMP mediated calcium influx. In the present study it is shown that E. coli STa inhibits cell proliferation in the colonic carcinoma cell line COLO-205 by the PKG-ERK44/42 mediated signaling pathway. This enterotoxin negatively regulates cell proliferation by downregulating the activity of ERK44/42(MAPK) and subsequently the activity of a transcription regulatory protein cMyc. The antiproliferative effect of STa was reversed by LY83583, a guanylate cyclase (GC) inhibitor and KT5823, a PKG inhibitor. Thus suggesting the involvement of cGMP dependent protein kinase (PKG) in the downregulation of ERK44/42 and subsequent inactivation of cMyc activity. Moreover, it has been shown that a specific ERK44/42 inhibitor, PD98059, also inhibits cMyc activation and cell proliferation, which further confirms theinvolvement of ERK44/42 in the activation of cMyc. It is also shown that E. coli STa significantly inhibits the vascular endothelial growth factor (VEGF, a potent angiogenic factor) expression in COLO-205 cells and also downregulates vascular cell adhesion molecule-1 (VCAM-1, a potent metastatic factor) expression on the COLO-205 cell surface. So it is reported for the first time that E. coli STa inhibits the proliferation of the colonic carcinoma cell line COLO-205 by the PKG-ERK44/42 mediated pathway and it may have a role against the development of colon carcinoma.
机译：早前有报道，分泌性腹泻的主要病原体大肠杆菌热稳定肠毒素（STa）也可以通过cGMP介导的钙内流而抑制结肠癌细胞的增殖。在本研究中，表明大肠杆菌STa通过PKG-ERK44 / 42介导的信号通路抑制结肠癌细胞系COLO-205中的细胞增殖。这种肠毒素通过下调ERK44 / 42（MAPK）的活性以及随后转录调节蛋白cMyc的活性来负调节细胞增殖。 STa的抗增殖作用被鸟苷酸环化酶（GC）抑制剂LY83583和PKG抑制剂KT5823逆转。因此提示cGMP依赖性蛋白激酶（PKG）参与ERK44 / 42的下调和cMyc活性的失活。此外，已经表明，特定的ERK44 / 42抑制剂PD98059也抑制cMyc的活化和细胞增殖，这进一步证实了ERK44 / 42参与cMyc的活化。还显示大肠杆菌STa显着抑制COLO-205细胞中的血管内皮生长因子（VEGF，有效的血管生成因子）表达，还下调了血管细胞粘附分子1（VCAM-1，有效的转移因子）表达在COLO-205细胞表面上。因此，首次报道大肠杆菌STa通过PKG-ERK44 / 42介导的途径抑制结肠癌细胞株COLO-205的增殖，并且可能对结肠癌的发展具有作用。

著录项

相似文献

  • 外文文献
  • 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