PI3K/AKT/mTOR通路
生物
蛋白激酶B
癌症研究
细胞生长
癌变
感染的多重性
信号转导
荧光素酶
分子生物学
细胞
细胞生物学
转染
细胞培养
基因
生物化学
遗传学
作者
Yan Yu,Dan Zhao,Kongfei Li,Yubo Cai,Penglin Xu,Rui Li,Juan Li,Xiaolong Chen,Ping Chen,Guangying Cui
标识
DOI:10.1038/s41419-020-2478-0
摘要
Abstract The DEAD/DEAH box helicase 11 (DDX11) plays vital roles in regulating the initiation of DNA replication. However, its precise function and regulation in hepatocellular carcinoma (HCC) have never been reported yet. In the current study, we found that DDX11 was overexpressed in HCC tissues. High DDX11 expression was positively correlated with large tumor size, tumor multiplicity, late tumor-node-metastasis (TNM) stage and poor prognosis. Additional, gain-of-function and loss-of-function experimental results revealed that DDX11 overexpression promoted HCC cell proliferation, migration, invasion and inhibited cell apoptosis in vitro. Overexpression of DDX11 also enhanced HCC tumorigenicity in vivo. Furthermore, DDX11 was transcriptionally regulated by transcription factor E2F1 in HCC, as demonstrated by chromatin immunoprecipitation (Ch-IP) and luciferase reporter assays. Mechanistically, E2F1/DDX11 axis promoted HCC cell proliferation, migration and invasion, at least in part, through activating PI3K/AKT/mTOR signaling pathway. Conclusively, our study demonstrates that E2F1-enhanced DDX11 expression promotes HCC progression through PI3K/AKT/mTOR pathway and DDX11 might be a potential therapeutic and prognostic target for HCC treatment.
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