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Knockdown of SALL4 Inhibits Proliferation, Migration, and Invasion in Osteosarcoma Cells

Dengfeng Zhang1, Feng Jiang1, Xiao Wang, Guojun Li

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

Oncology Research 2017, 25(5), 763-771. https://doi.org/10.3727/096504016X14772402056137

Abstract

Sal-like protein 4 (SALL4) is a zinc finger transcription factor that has been reported to be aberrantly expressed in several human malignancies and identified as an oncogene. However, the potential role of SALL4 in osteosarcoma remains to be elucidated. In this study, we explored the biological functions of SALL4 in osteosarcoma. We found that SALL4 was overexpressed in osteosarcoma tissues and cell lines. Knockdown of SALL4 inhibited osteosarcoma cell proliferation, migration, and invasion in vitro. In addition, SALL4 knockdown suppressed osteosarcoma growth and metastasis in vivo. We also showed that SALL4 knockdown decreased the protein expression of Wnt3a and b-catenin in osteosarcoma cells. Taken together, our study showed that SALL4 plays an important role in regulating the proliferation, migration, and invasion of osteosarcoma cells. Thus, SALL4 may represent a potential therapeutic target in the treatment of osteosarcoma.

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APA Style
Zhang, D., Jiang, F., Wang, X., Li, G. (2017). Knockdown of SALL4 inhibits proliferation, migration, and invasion in osteosarcoma cells. Oncology Research, 25(5), 763-771. https://doi.org/10.3727/096504016X14772402056137
Vancouver Style
Zhang D, Jiang F, Wang X, Li G. Knockdown of SALL4 inhibits proliferation, migration, and invasion in osteosarcoma cells. Oncol Res. 2017;25(5):763-771 https://doi.org/10.3727/096504016X14772402056137
IEEE Style
D. Zhang, F. Jiang, X. Wang, and G. Li, “Knockdown of SALL4 Inhibits Proliferation, Migration, and Invasion in Osteosarcoma Cells,” Oncol. Res., vol. 25, no. 5, pp. 763-771, 2017. https://doi.org/10.3727/096504016X14772402056137



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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