Open Access

ARTICLE

Knockdown of DDX5 Inhibits the Proliferation and Tumorigenesis in Esophageal Cancer

Zhenchuan Ma^*, Jie Feng^†, Yurui Guo^‡, Ranran Kong^*, Yuefeng Ma^*, Liangzhang Sun^*, Xiaoping Yang^*, Bin Zhou^*, Shaomin Li^*, Wei Zhang^*, Jiantao Jiang^*, Jin Zhang^*, Zhe Qiao^*, Yao Cheng^*, Danjie Zha^*, Shiyuan Liu^*

* Department of Thoracic Surgery, The Second Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, Shaanxi, P.R. China
† Department of Nephrology, The First Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, Shaanxi, P.R. China
‡ Department of Anesthesia, The Second Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, Shaanxi, P.R. China

Oncology Research 2017, 25(6), 887-895. https://doi.org/10.3727/096504016X14817158982636

Abstract

DEAD (Asp-Glu-Ala-Asp) box protein 5 (DDX5), a prototypical member of the DEAD/H-box protein family, has been involved in several human malignancies. However, the expression and biological role of DDX5 in esophageal cancer (EC) remain largely unknown. In this study, we examined the role of DDX5 in regulating EC cell proliferation and tumorigenesis and explored its possible molecular mechanism. We found that DDX5 was overexpressed in human EC cell lines. In addition, knockdown of DDX5 significantly inhibited the proliferation of EC cells in vitro and the growth of EC xenografts in vivo. Knockdown of DDX5 also suppressed the migration/invasion and epithelial-to-mesenchymal transition (EMT) phenotype in EC cells. Furthermore, we observed that knockdown of DDX5 inhibited the expression of β-catenin, c-Myc, and cyclin D1 in EC cells. In conclusion, our findings provide the first evidence that siRNA-DDX5 inhibited the proliferation and invasion of EC cells through suppressing the Wnt/β-catenin signaling pathway. Therefore, DDX5 may be a novel potential therapeutic target for the prevention and treatment of EC.

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