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

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


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.

Original languageEnglish
Pages (from-to)887-895
Number of pages9
JournalOncology Research
Issue number6
StatePublished - 2017
Externally publishedYes


  • DEAD (Asp-Glu-Ala-Asp) box protein 5 (DDX5)
  • Esophageal cancer (EC)
  • Invasion
  • Proliferation


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