Oncotarget

Research Papers:

POU2F1 over-expression correlates with poor prognoses and promotes cell growth and epithelial-to-mesenchymal transition in hepatocellular carcinoma

Yonghao Zhong, Hongyang Huang, Min Chen, Jinzhou Huang, Qingxia Wu, Guang-Rong Yan _ and De Chen

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Oncotarget. 2017; 8:44082-44095. https://doi.org/10.18632/oncotarget.17296

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Abstract

Yonghao Zhong1,2,*, Hongyang Huang1,2,*, Min Chen1, Jinzhou Huang1, Qingxia Wu1, Guang-Rong Yan1,3 and De Chen1,2,3

1Biomedicine Research Center, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China

2Department of Surgery, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China

3Key Laboratory of Protein Modification and Degradation, Guangzhou Medical University, Guangzhou, China

*These authors have contributed equally to this work

Correspondence to:

Guang-Rong Yan, email: [email protected]

De Chen, email: [email protected]

Keywords: POU2F1, hepatocellular carcinoma

Abbreviations: POU2F1, POU domain class 2 transcription factor 1; HCC, hepatocellular carcinoma; EMT, epithelial-to-mesenchymal transition; OS, overall survival

Received: November 11, 2016     Accepted: April 03, 2017     Published: April 20, 2017

ABSTRACT

Despite recent efforts to understand activities of POU domain class 2 transcription factor 1 (POU2F1), little is known about the roles of POU2F1 in hepatocellular carcinoma (HCC) tumorigenesis and its correlation with any clinicopathological feature of HCC. In this study, we found that POU2F1 was significantly up-regulated in HCC specimens compared with adjacent non-cancerous liver specimens. The high POU2F1 protein expression level positively correlated with large tumor size, high histological grade, tumor metastasis and advanced clinical stage, and HCC patients with high POU2F1 levels exhibited poor prognoses. We further demonstrated that POU2F1 over-expression promoted HCC cell proliferation, colony formation, epithelial-to-mesenchymal transition (EMT), migration and invasion, while silencing of POU2F1 inhibited these malignant phenotypes. POU2F1 induced the expression of Twist1, Snai1, Snai2 and ZEB1 genes which are involved in the regulation of EMT. Furthermore, POU2F1 was up-regulated by AKT pathway in HCC, and POU2F1 over-expression reversed the inhibition of malignant phenotypes induced by AKT knock-down, indicating POU2F1 is a key down-stream effector of AKT pathway. Collectively, our results indicate that POU2F1 over-expression is positively associated with aggressive phenotypes and poor survival in patients with HCC, and POU2F1 regulated by AKT pathway promotes HCC aggressive phenotypes by regulating the transcription of EMT genes. POU2F1 may be employed as a new prognostic factor and therapeutic target for HCC.


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