自噬
PI3K/AKT/mTOR通路
蛋白激酶B
上皮-间质转换
癌症研究
信号转导
细胞生长
生物
污渍
下调和上调
细胞生物学
化学
细胞凋亡
遗传学
生物化学
基因
作者
Kaida Huang,Yu-biao Lin,Keyin Wang,Shen Jian-fen,Dahai Wei
摘要
Our results substantiate a novel mechanism by which ARFIP2 can regulate the activity/phosphorylation of Akt to promote EMT and inhibit autophagy in part via the PI3K/Akt signalling pathway. The ARFIP2/PI3K/Akt axis may be a potential diagnostic biomarker and therapeutic target for HCC.
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