Analysis of the PI3K pathway in colon cancer and new strategy of Molecular target-based drugs.

结肠癌PI3K通路分析及分子靶点药物新策略

• 批准号: 21591721
• 负责人: SUNAMI Eiji
• 金额: $ 2.83万
• 依托单位: The University of Tokyo
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21591721/
• 关键词: 大腸癌; 化学療法; mTOR; Rapamycin; 多剤併用療法; 癌; シグナル伝達; PI3K-Akt経路; MAPキナーゼ経路

We demonstrated that Tesirolimus cause G1 cell cycle arrest in colon cancer cell lines with inhibition of cyclin D1 protein production. Furthermore, we also indicated that Tesirolimus inhibits production of Hypoxia-inducible factor-alpha protein of colon cancer cell lines under the environment of hypoxia. Those explications of the mechanisms of Tesirolimus against cancer proliferation may play an important role in the selection of anticancer agents for colon cancer.

我们证明了Tesirolimus在结肠癌细胞系中引起G1细胞周期停滞，并抑制细胞周期蛋白D1蛋白的产生。此外，我们还指出，在缺氧环境下，Tesirolimus抑制结肠癌细胞系缺氧诱导因子-Alpha蛋白的产生。那些针对癌症增殖机制的解释可能在选择结肠癌的抗癌剂中起重要作用。

项目成果

Temsirolimus inhibits colon cancer growth in vitro and in vivo

• DOI: 10.1158/1538-7445.am2012-2819
• 发表时间: 2012-04-15
• 期刊: CANCER RESEARCH
• 影响因子: 11.2
• 作者: Kaneko, Manabu;Nozawa, Hiroaki;Kitayama, Joji
• 通讯作者: Kitayama, Joji