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Elevated eukaryotic elongation factor 2 expression is involved in proliferation and invasion of lung squamous cell carcinoma

Yang Song, Bing Sun, LiHong Hao, Jun Hu, Sha Du, Xin Zhou, LiYuan Zhang, Lu Liu, LinLin Gong, XinMing Chi, Qiang Liu and ShuJuan Shao _

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Oncotarget. 2016; 7:58470-58482. https://doi.org/10.18632/oncotarget.11298

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Abstract

Yang Song1,*, Bing Sun2,*, LiHong Hao1, Jun Hu1, Sha Du3, Xin Zhou1, LiYuan Zhang1, Lu Liu1, LinLin Gong1, XinMing Chi1, Qiang Liu3, ShuJuan Shao1,4

1Department of Histology and Embryology, Dalian Medical University, Dalian, China

2Department of Chest Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian, China

3Institute of Cancer Stem Cell, Dalian Medical University Cancer Center, Liaoning, China

4Liaoning Key Laboratory of Proteomics, Dalian Medical University, Liaoning, China

*These authors have contributed equally to this work

Correspondence to:

Shujuan Shao, email: [email protected]

Keywords: eukaryotic elongation factor 2, lung squamous cell carcinoma, proliferation, invasion, proteomics

Received: March 16, 2016    Accepted: July 27, 2016    Published: August 16, 2016

ABSTRACT

Eukaryotic elongation factor 2 (EF2), is a critical enzyme solely responsible for catalyzing the translocation of the elongated peptidyl-tRNA from the A to P sites of the ribosome during the process of protein synthesis. EF2 is found to be highly expressed in a variety of malignant tumors and is correlated with cancer cell progression and recurrence. The present study was designed to uncover the function of EF2 on lung squamous cell carcinoma (LSCC) cancer cell growth and progression. Our results from clinical tissue studies showed that EF2 protein was significantly overexpressed in LSCC tissues, compared with the adjacent normal lung tissues, which was confirmed by western blotting and tissue microarray. Forced expression of EF2 resulted in the enhancement of lung squamous carcinoma NCI-H520 cells growth through promotion of G2/M progression in cell cycle, activating Akt and Cdc2/Cyclin B1. In nude mice cancer xenograft model, overexpression of EF2 significantly facilitated cell proliferation in vivo. Furthermore, forced expression of EF2 in the cells increased the capabilities of migration and invasion by changing the expressions of EMT-related proteins and genes. These results provided novel insights into the role of EF2 in tumorigenesis and progression in LSCC. EF2-targeted therapy could become a good strategy for the clinical treatment of LSCC.


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