Research Papers:

AGK enhances angiogenesis and inhibits apoptosis via activation of the NF-κB signaling pathway in hepatocellular carcinoma

Yanmei Cui _, Chuyong Lin, Zhiqiang Wu, Aibin Liu, Xin Zhang, Jinrong Zhu, Geyan Wu, Jueheng Wu, Mengfeng Li, Jun Li and Libing Song

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Oncotarget. 2014; 5:12057-12069. https://doi.org/10.18632/oncotarget.2666

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Yanmei Cui1,*, Chuyong Lin1,*, Zhiqiang Wu2,*, Aibin Liu2, Xin Zhang1, Jinrong Zhu2, Geyan Wu2, Jueheng Wu3, Mengfeng Li3, Jun Li2, Libing Song1

1State Key Laboratory of Oncology in Southern China, Department of Experimental Research, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, China

2Department of Biochemistry, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, China

3Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, Guangdong 510080, China

*These authors contributed equally to this work

Correspondence to:

Libing Song, e-mail: [email protected]

Jun Li, e-mail: [email protected]

Keywords: AGK, Hepatocellular carcinoma, Angiogenesis, Apoptosis, NF-κB signaling

Received: October 04, 2014     Accepted: October 28, 2014     Published: November 29, 2014


High levels of angiogenesis and resistance to apoptosis are major clinical features of hepatocellular carcinoma (HCC), a lethal disease with a high incidence worldwide. However, the precise mechanisms underlying these malignant properties remain unclear. Here, we demonstrated that acylglycerol kinase (AGK) is markedly overexpressed in HCC cell lines and clinical tissues. Immunohistochemical analysis of 245 clinical HCC specimens revealed patients with high levels of AGK expression had poorer overall survival compared to patients with low AGK expression. Furthermore, overexpressing AGK significantly enhanced angiogenesis and inhibited apoptosis in vitro and promoted the tumorigenicity of HCC cells in vivo; silencing endogenous AGK had the opposite effects. Importantly, AGK enhanced angiogenesis and inhibited apoptosis in HCC in part via activation of NF-κB signaling. Our findings provide new evidence that AGK plays an important role in promoting angiogenesis and providing resistance to apoptosis, thus AGK may represent a novel therapeutic target for HCC.

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