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

在体外，AICAR显著降低恶性间皮瘤(MM)细胞的增殖率。在体内，AICAR显著降低了MM的生长速度，并伴随着P53/P53蛋白水平的升高，以及P53/P53和P70/P70蛋白水平的下调。在体外实验中也观察到了类似的细胞内通路。这些作用部分涉及诱导多发性骨髓瘤细胞的生长停滞和凋亡。AICAR处理激活了AMPK。最后，AICAR治疗还显著延长了MM植入性动物模型的生存时间。这些发现表明，AICAR或AMPK活性的诱导是发展MM治疗策略的重要策略。

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.