Research Papers:

Functional role of eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) in NSCLC

Yueyu Cao, Mengdan Wei, Bing Li, Yali Liu, Ying Lu, Zhipeng Tang, Tianbao Lu, Yujiao Yin, Zhiqiang Qin _ and Zengguang Xu

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Oncotarget. 2016; 7:24242-24251. https://doi.org/10.18632/oncotarget.8168

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Yueyu Cao1,3, Mengdan Wei2,3, Bing Li2,3, Yali Liu2,3, Ying Lu2,3, Zhipeng Tang1,3, Tianbao Lu3, Yujiao Yin1,3, Zhiqiang Qin1,2,3,4, Zengguang Xu2,3

1Department of Oncology, Shanghai East Hospital, Dalian Medical University, Shanghai 200120, China

2Department of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China

3Research Center for Translational Medicine and Key Laboratory of Arrhythmias, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, China

4Departments of Microbiology/Immunology/Parasitology, Louisiana State University Health Sciences Center, Louisiana Cancer Research Center, New Orleans, LA 70112, USA

Correspondence to:

Zhiqiang Qin, e-mail: zqin@lsuhsc.edu

Zengguang Xu, e-mail: xuzg1998@163.com

Keywords: EIF4G1, USP10, NSCLC, lung cancer

Received: January 26, 2016     Accepted: March 02, 2016     Published: March 18, 2016


Eukaryotic translation initiation factor 4 gamma 1(EIF4G1) is related to tumorigenesis and tumor progression. However, its role and the underlying mechanisms in the regulation of tumor development in non–small cell lung cancers (NSCLC) remain largely unknown. Here we report that the levels of EIF4G1 expression are much higher in NSCLC cell lines and tumor tissues than those in the normal lung cells and adjacent normal tissues from the same patients. Using shRNA to knock down EIF4G1 expression stably, we found EIF4G1 required for NSCLC cell proliferation, anchorage-independent growth, migration and invasion. Furthermore, silencing of EIF4G1 induces NSCLC cell apoptosis and causes G0/G1 cell cycle arrest. To identify the partner protein network of EIF4G1 in NSCLC cells, we found that Ubiquitin-specific protease 10 (USP10) can directly interacts with EIF4G1, while acting as a negative regulator for EIF4G1-mediated functions. Together, our results indicate that EIF4G1 functions as an oncoprotein during NSCLC development, which may represent a novel and promising therapeutic target in lung cancer.

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