@Article{096504016X14817158982636,
AUTHOR = {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},
TITLE = {Knockdown of DDX5 Inhibits the Proliferation  and Tumorigenesis in Esophageal Cancer},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {6},
PAGES = {887--895},
URL = {http://www.techscience.com/or/v25n6/56871},
ISSN = {1555-3906},
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.},
DOI = {10.3727/096504016X14817158982636}
}