Oncotarget

Research Papers:

Mammalian Eps15 homology domain 1 promotes metastasis in non-small cell lung cancer by inducing epithelial-mesenchymal transition

Qingwei Meng, Ying Xing, Tingting Ren, Hailing Lu, Yuhui Xi, Zhijun Jiang, Jing Hu, Chunhong Li, Lichun Sun, Dianjun Sun and Li Cai _

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Oncotarget. 2017; 8:22433-22442. https://doi.org/10.18632/oncotarget.11220

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Abstract

Qingwei Meng1,2,*, Ying Xing1,*, Tingting Ren2, Hailing Lu1, Yuhui Xi3, Zhijun Jiang3, Jing Hu1, Chunhong Li1, Lichun Sun1, Dianjun Sun4, Li Cai1

1The Fourth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin 150040, China

2The Sixth Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin 150040, China

3Department of Pathophysiology, Harbin Medical University, Harbin 150081, China

4The Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, China

*These authors contributed equally to this work and should be regarded as joint first authors

Correspondence to:

Li Cai, email: caili@ems.hrbmu.edu.cn

Keywords: EHD1, non-small cell lung cancer, metastasis, epithelial-mesenchymal transition

Received: May 13, 2016    Accepted: July 14, 2016    Published: August 11, 2016

ABSTRACT

The identification of the earliest molecular events responsible for the metastatic dissemination of non-small cell lung cancer (NSCLC) remains critical for early detection, prevention, and treatment interventions. In this study, we hypothesized that Mammalian Eps15 homology domain 1 (EHD1) might be responsible for the metastatic behavior of cells in NSCLC. We demonstrated that upregulation of EHD1 is associated with lymph nodes metastasis and unfavorable survival in patients with NSCLC. EHD1 knockdown inhibited the invasion and migration of human NSCLC cells, and overexpression of EHD1 increased the metastatic potential of lung cancer cells. Using the Affymetrix Human Gene 1.0 ST platform, microarray analysis revealed that an association between EHD1 and epithelial-mesenchymal transition (EMT), supported by downregulation of mesenchymal markers and upregulation of epithelial markers following knockdown of EHD1 in cell lines. Moreover, overexpression of EHD1 induced the EMT and increased the metastatic potential of lung cancer cells in vitro and in vivo. These results provide a model to illustrate the relationship between EHD1 expression and lung cancer metastasis, opening up new avenues for the prognosis and therapy of lung cancer.


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