Oncotarget

Research Papers:

UBE2T promotes nasopharyngeal carcinoma cell proliferation, invasion, and metastasis by activating the AKT/GSK3β/β-catenin pathway

Wei Hu, Lushan Xiao, Chuanhui Cao, Shengni Hua and Dehua Wu _

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Oncotarget. 2016; 7:15161-15172. https://doi.org/10.18632/oncotarget.7805

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Abstract

Wei Hu1,*, Lushan Xiao2,*, Chuanhui Cao1, Shengni Hua1, Dehua Wu1

1Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China

2Department of Infectious Diseases and Hepatology Unit, Nanfang Hospital, Southern Medical University, Guangzhou, China

*These authors have contributed equally to this work

Correspondence to:

Dehua Wu, e-mail: [email protected]

Keywords: nasopharyngeal carcinoma, UBE2T, proliferation, metastasis, AKT/GSK3β/β-catenin pathway

Received: September 02, 2015    Accepted: January 29, 2016    Published: March 01, 2016

ABSTRACT

Increasing evidence has shown that UBE2T plays an important role in genomic integrity and carcinogenesis; however, its role in nasopharyngeal carcinoma (NPC) has not been investigated. Here, we evaluated the clinicopathological significance of UBE2T in NPC and its underlying mechanisms. Using immunohistochemical analysis of UBE2T expression in NPC samples, we demonstrated that UBE2T is highly expressed in NPC tissues, which correlated with the T/M classification, skull invasion, and poor prognosis. The in vitro assay showed that UBE2T overexpression promoted proliferation, migration, and invasion of NPC cells, while UBE2T knockdown inhibited these processes. Consistent with our in vitro results, in vivo studies indicated that UBE2T overexpression promoted the growth of NPC xenografts and NPC cell metastasis. We found that UBE2T overexpression activated, whereas UBE2T knockdown inhibited, the AKT/GSK3β/β-catenin pathway. Moreover, the pathway-activation and in vitro pro-metastasis effects of UBE2T were blocked by the AKT inhibitor, MK-2206 2HCl. Additionally, UBE2T and p-GSK3 β co-expressed in NPC samples by serial section, and their expressions are correlated. Collectively, our findings demonstrated that UBE2T is a possible diagnostic/prognostic biomarker for NPC and may promote the development and progression of NPC by activating the AKT/GSK3β/β-catenin pathway. Thus, UBE2T could serve as an alternative target for the treatment of NPC.


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