姜黄素
自噬
PI3K/AKT/mTOR通路
蛋白激酶B
生物
信号转导
细胞凋亡
细胞生物学
激酶
细胞毒性
程序性细胞死亡
癌症研究
药理学
体外
生物化学
作者
Naoki Shinojima,Tomohisa Yokoyama,Yasuko Kondo,Seiji Kondo
出处
期刊:Autophagy
[Informa]
日期:2007-11-26
卷期号:3 (6): 635-637
被引量:296
摘要
Curcumin has a potent anticancer effect and is a promising new therapeutic strategy. We previously demonstrated that curcumin induced non-apoptotic autophagic cell death in malignant glioma cells in vitro and in vivo. This compound inhibited the Akt/mammalian target of rapamycin/p70 ribosomal protein S6 kinase pathway and activated the extracellular signal-regulated kinases 1/2 thereby inducing autophagy. Interestingly, activation of the first pathway inhibited curcumin-induced autophagy and cytotoxicity, whereas inhibition of the latter pathway inhibited curcumin-induced autophagy and induced apoptosis, thus augmenting the cytotoxicity of curcumin. These results imply that these two autophagic pathways have opposite effects on curcumin's cytotoxicity. However, inhibition of nuclear factor kappaB, which is the main target of curcumin for its anticancer effect, was not observed in malignant glioma cells. These results suggest that autophagy but not nuclear factor kappaB plays a central role in curcumin anticancer therapy and warrant further investigation toward application in patients with malignant gliomas. Here, we discuss the therapeutic role of two autophagic pathways influenced by curcumin.
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