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Knockdown of DDX46 Inhibits the Invasion and Tumorigenesis in Osteosarcoma Cells

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Department of Orthopedics, Huaihe Hospital of Henan University, Kaifeng, Henan Province, P.R. China
1 These authors provided equal contribution to this work.

Oncology Research 2017, 25(3), 417-425. https://doi.org/10.3727/096504016X14747253292210

Abstract

DDX46, a member of the DEAD-box (DDX) helicase family, is involved in the development of several tumors. However, the exact role of DDX46 in osteosarcoma and the underlying mechanisms in tumorigenesis remain poorly understood. Thus, in the present study, we explored the role of DDX46 in osteosarcoma and the underlying mechanisms. Our results demonstrated that the expression levels of DDX46 in both mRNA and protein were greatly elevated in human osteosarcoma tissues and cell lines. Knockdown of DDX46 obviously inhibited osteosarcoma cell proliferation and tumor growth in vivo. In addition, knockdown of DDX46 also significantly suppressed migration and invasion in osteosarcoma cells. Furthermore, knockdown of DDX46 substantially downregulated the phosphorylation levels of PI3K and Akt in SaOS2 cells. In summary, the present results have revealed that DDX46 plays an important role in osteosarcoma growth and metastasis. Knockdown of DDX46 inhibited osteosarcoma cell proliferation, migration, and invasion in vitro and tumor growth in vivo. Therefore, DDX46 may be a potential therapeutic target for the treatment of osteosarcoma.

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APA Style
Jiang, F., Zhang, D., Li, G., Wang, X. (2017). Knockdown of DDX46 inhibits the invasion and tumorigenesis in osteosarcoma cells. Oncology Research, 25(3), 417-425. https://doi.org/10.3727/096504016X14747253292210
Vancouver Style
Jiang F, Zhang D, Li G, Wang X. Knockdown of DDX46 inhibits the invasion and tumorigenesis in osteosarcoma cells. Oncol Res. 2017;25(3):417-425 https://doi.org/10.3727/096504016X14747253292210
IEEE Style
F. Jiang, D. Zhang, G. Li, and X. Wang, “Knockdown of DDX46 Inhibits the Invasion and Tumorigenesis in Osteosarcoma Cells,” Oncol. Res., vol. 25, no. 3, pp. 417-425, 2017. https://doi.org/10.3727/096504016X14747253292210



cc Copyright © 2017 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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