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CPEB4 promotes growth and metastasis of gastric cancer cells via ZEB1-mediated epithelial–mesenchymal transition

Authors Cao G, Chen D, Liu G, Pan Y, Liu Q

Received 26 May 2018

Accepted for publication 5 July 2018

Published 21 September 2018 Volume 2018:11 Pages 6153—6165


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Sanjeev Srivastava

Gan Cao,* Dehu Chen,* Guiyuan Liu, Yan Pan, Qinghong Liu

Department of General Surgery, Taizhou People’s Hospital, The Fifth Affiliated Hospital of Nantong University, Taizhou 225300, People’s Republic of China

*These authors contributed equally to this work

Background: Cytoplasmic polyadenylation element-binding protein 4 (CPEB4) has previously been reported to be associated with biological malignancy in various cancers. However, its function in tumor growth and metastasis in gastric cancer (GC) remains obscure. Here, we explored the functional and molecular mechanisms by which CPEB4 influences GC.
Materials and methods: The expression of CPEB4 was assessed using Western blot and immunohistochemistry in GC specimens. The roles of CPEB4 in GC cell proliferation, migration, and invasion were investigated by cell-counting kit-8 (CCK-8), colony formation, and EdU assay; wound-healing assay; and transwell assay, respectively. Quantitative real-time PCR (qRT-PCR), Western blot, and immunofluorescence staining were performed to detect the expressions of CPEB4 and epithelial–mesenchymal transition (EMT)-related markers. The function of CPEB4 on GC cell growth and metastasis was also determined in vivo through establishing subcutaneous xenograft tumor and lung metastatic mice model.
Results: The results revealed that the expression of CPEB4 was increased in GC tissues compared with matched normal tissues. High expression level of CPEB4 was significantly associated with clinical metastasis and unfavorable prognosis in patients with GC. Furthermore, CPEB4 silencing remarkably inhibited GC cells’ proliferation, invasion, and metastasis in vitro and in vivo. Conversely, CPEB4 overexpression achieved the opposite effects. Mechanically, we proved that ZEB1-mediated EMT might be involved in CPEB4-facilitated GC cells’ proliferation, invasion, and metastasis.
Conclusion: Our findings implied that CPEB4 expression predicted a worse prognosis in patients with GC. Besides, CPEB4 contributed to GC cells’ proliferation, migration, and invasion via ZEB1-mediated EMT.

Keywords: CPEB4, gastric cancer, epithelial–mesenchymal transition

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