Elevated expression of eukaryotic translation initiation factor 3H is associated with proliferation, invasion and tumorigenicity in human hepatocellular carcinoma
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Qian Zhu1,*, Guo-Liang Qiao2,*, Xiao-Chuan Zeng1,*, Yun Li1, Jian-Jun Yan3, Rui Duan1, Zhi-Yong Du4
1Department of General Surgery, Jingmen First People's Hospital, Jingmen 448000, Hubei Province, China
2Department of Medical Oncology, Capital Medical University Cancer Center, Beijing Shijitan Hospital, Beijing, 100038, China
3First Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, China
4Department of Hepatobiliary Surgery, Central Hospital of Wuhan, Wuhan 430014, Hubei Province, China
*These authors have contributed equally to this work
Zhi-Yong Du, email: [email protected]
Rui Duan, email: [email protected]
Keywords: hepatocellular carcinoma, initiation factors, microarray, prognosis, tumor progression
Received: October 07, 2015 Accepted: June 04, 2016 Published: June 22, 2016
Aim: We studied the role of eukaryotic translation initiation factor 3 subunit H (EIF3H) in hepatocellular carcinoma (HCC) progression.
Results: High EIF3H expression was observed in 50.23% patients. Upregulation of EIF3H is an independent predictor for greater rates of cancer recurrence and shorter overall survival in HCC patients. Knockdown of EIF3H expression in HCC cells promoted apoptosis, and inhibited cell growth, colony formation, migration, as well as xenograft growth. TGF-βand MAPK pathways are potentially targeted by EIF3H.
Methods: EIF3H mRNA expression was measured in HCC tissue samples and paired non-tumor samples (N=60) and results were validated in another dataset of 215 HCC patients. Then EIF3H expression and clinical outcomes were correlated. Malignant phenotypes were studied after EIF3H expression was knocked down with siRNA in HCC cell lines. EIF3H targeted pathways were identified by microarray analysis.
Conclusion: EIF3H is frequently upregulated and is an independent prognostic marker for HCC patients and EIF3H inhibition mitigates the malignant phenotype. Our data provide novel insight into the function of EIF3H in HCC progression, and suggest that EIF3H may be a potentially valuable biomarker for HCC.
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