The effect of 5-aminoimidazole-4-carboxamide ribonucleoside (AMPK)on malignant mesothelioma cell growth and survival interval in an implant animal model of malignant mesothelioma

5-氨基咪唑-4-甲酰胺核糖核苷（AMPK）对恶性间皮瘤移植动物模型中恶性间皮瘤细胞生长和生存期的影响

• 批准号: 21790763
• 负责人: NIU Kaijun
• 金额: $ 2.66万
• 依托单位: Tohoku University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 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-21790763/
• 关键词: 非閉塞性肺疾患癌; 肺線維症; 呼吸器感染症; ヒト悪性中皮腫; 悪性中皮腫; AMPK活性; AICAR; SCIDマウス; 細胞周期; アポトーシス; AMPK活性化

In vitro, AICAR treatment significantly impaired the cell proliferation rate of malignant mesothelioma (MM)cell lines. In vivo, treatment with AICAR significantly decreased the growth rate of MM, which was accompanied by an increase in p53/phosphor-p53 levels, and down-regulated protein levels of phosphor-Akt and p70/phosphor-p70. Similar intracellular pathways are also observed in vitro experiment. These effects partly involved induction of growth arrest and apoptosis to MM cells. AICAR treatment activated AMPK. Finally, AICAR treatment also significantly extended survival interval in an implant animal model of MM. These findings suggested that AICAR or the induction of AMPK activity is an important tactic for developing therapeutic strategies against MM.

在体外实验中，AICAR处理显著降低了恶性间皮瘤（MM）细胞系的细胞增殖率。在体内，AICAR治疗显著降低MM的生长速度，同时p53/磷酸化-p53水平升高，磷酸化- akt和磷酸化-p70蛋白水平下调。在体外实验中也观察到类似的细胞内通路。这些作用部分涉及诱导MM细胞生长停滞和凋亡。AICAR处理激活了AMPK。最后，AICAR治疗还显著延长了MM植入动物模型的生存期。这些发现表明，AICAR或诱导AMPK活性是开发MM治疗策略的重要策略。

项目成果

Adiponectin pathway attenuates malignant mesothelioma cell growth.

• DOI: 10.1165/rcmb.2011-0068oc
• 发表时间: 2012-12
• 期刊: American journal of respiratory cell and molecular biology
• 影响因子: 6.4
• 作者: K. Niu;M. Asada;Tatsuma Okazaki;S. Yamanda;T. Ebihara;Hui Guo;Dongyin Zhang;R. Nagatomi;H. Arai;M. Kohzuki;S. Ebihara

AMP活性化プロテインキナーゼ活性化と悪性中皮腫

AMP 激活蛋白激酶激活与恶性间皮瘤

• 发表时间: 2010
• 作者: 牛凱軍;海老原覚;浅田成紀;矢満田慎介;岡崎達馬;荒井啓行;永富良一
• 通讯作者: 永富良一