合成代谢
PI3K/AKT/mTOR通路
细胞保护
重编程
谷氨酰胺
蛋白激酶B
细胞生物学
代谢途径
生物
调节器
细胞生长
信号转导
mTORC1型
新陈代谢
细胞
细胞凋亡
生物化学
氨基酸
基因
作者
Yoichiro Mitsuishi,Keiko Taguchi,Yukie Kawatani,Tatsuhiro Shibata,Toshihiro Nukiwa,Hiroyuki Aburatani,Masayuki Yamamoto,Hozumi Motohashi
出处
期刊:Cancer Cell
[Elsevier]
日期:2012-07-01
卷期号:22 (1): 66-79
被引量:1106
标识
DOI:10.1016/j.ccr.2012.05.016
摘要
Cancer cells consume large quantities of nutrients and maintain high levels of anabolism. Recent studies revealed that various oncogenic pathways are involved in modulation of metabolism. Nrf2, a key regulator for the maintenance of redox homeostasis, has been shown to contribute to malignant phenotypes of cancers including aggressive proliferation. However, the mechanisms with which Nrf2 accelerates proliferation are not fully understood. Here, we show that Nrf2 redirects glucose and glutamine into anabolic pathways, especially under the sustained activation of PI3K-Akt signaling. The active PI3K-Akt pathway augments the nuclear accumulation of Nrf2 and enables Nrf2 to promote metabolic activities that support cell proliferation in addition to enhancing cytoprotection. The functional expansion of Nrf2 reinforces the metabolic reprogramming triggered by proliferative signals.
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