Oncotarget

Research Papers:

Overexpression of Semaphorin-3E enhances pancreatic cancer cell growth and associates with poor patient survival

Lin-Kin Yong, Syeling Lai, Zhengdong Liang, Ethan Poteet, Fengju Chen, George van Buren, William Fisher, Qianxing Mo, Changyi Chen and Qizhi Yao _

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Oncotarget. 2016; 7:87431-87448. https://doi.org/10.18632/oncotarget.13704

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Abstract

Lin-Kin Yong1,2, Syeling Lai3, Zhengdong Liang1, Ethan Poteet1, Fengju Chen4,5, George van Buren4,6, William Fisher4,6, Qianxing Mo4,5, Changyi Chen1,4, Qizhi Yao1,4,7

1Michael E. DeBakey Department of Surgery, Division of Surgical Research, Baylor College of Medicine, Houston, TX, USA

2Interdepartmental Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, TX, USA

3Department of Pathology, Michael E. DeBakey VA Medical Center and Baylor College of Medicine, Houston, TX, USA

4Duncan Cancer Center, Baylor College of Medicine, Houston, TX, USA

5Department of Medicine, Baylor College of Medicine, Houston, TX, USA

6Michael E. DeBakey Department of Surgery, Division of General Surgery, Baylor College of Medicine, Houston, TX, USA

7Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, TX, USA

Correspondence to:

Qizhi Yao, email: qizhiyao@bcm.edu

Keywords: semaphorin 3E, pancreatic cancer

Received: July 05, 2016     Accepted: October 17, 2016     Published: November 29, 2016

ABSTRACT

Semaphorin-3E (Sema3E) is a member of an axon guidance gene family, and has recently been reported to contribute to tumor progression and metastasis. However, its role in pancreatic cancer is yet unknown and uncharacterized. In this study, we showed that Sema3E is overexpressed in human pancreatic cancer, and that high Sema3E levels are associated with tumor progression and poor survival. Interestingly, we also observed Sema3E expression in the nucleus, even though Sema3E is reported to be a secreted protein. Overexpression of Sema3E in pancreatic cancer cells promoted cell proliferation and migration in vitro, and increased tumor incidence and growth in vivo. Conversely, knockout of Sema3E suppressed cancer cell proliferation and migration in vitro, and reduced tumor incidence and size in vivo. Moreover, Sema3E induced cell proliferation via acting through the MAPK/ERK pathway. Collectively, these results reveal an undiscovered role of Sema3E in promoting pancreatic cancer pathogenesis, suggesting that Sema3E may be a suitable prognostic marker and therapeutic target for pancreatic cancer.


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