Rapamycin induces p53-independent apoptosis through the mitochondrial pathway in non-small cell lung cancer cells

作者: NAOMI MIYAKE , HIROKI CHIKUMI , MIYAKO TAKATA , MASAKI NAKAMOTO , TADASHI IGISHI

DOI: 10.3892/OR.2012.1855

关键词:

摘要: The mammalian target of rapamycin (mTOR) is a key kinase acting downstream growth factor receptor PI3K and AKT signaling, leading to processes resulting in increased cell size proliferation through translation control. Rapamycin, specific inhibitor mTOR, results predominately G1 cycle arrest control occasionally, type-dependent apoptosis by an unknown mechanism. In this study, we investigated the effect mechanism action on non-small lung cancer (NSCLC) lines with p53 mutations. Cell was evaluated modified MTT assay. apoptotic measured caspase-3 activation flow cytometric analysis Annexin V binding. expression Bcl-2 release cytochrome c from mitochondria were western blotting. We found that induced NSCLC Western blot demonstrated downregulates levels Bcl-2, which leads cytochrome c subsequent caspase cascades. These findings suggest induces p53-independent downregulation mitochondrial pathway as novel antitumor

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