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Overexpression of Aristaless-Like Homeobox-4 Inhibits Proliferation, Invasion, and EMT in Hepatocellular Carcinoma Cells

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* Control of Nosocomial Infections, Hong-hui Hospital, Xi’an Jiaotong University College of Medicine, Xi’an, P.R. China
† Department of Surgery, Hong-hui Hospital, Xi’an Jiaotong University College of Medicine, Xi’an, P.R. China
‡ Basic Medical College of Xi’an Jiaotong University, Xi’an, P.R. China

Oncology Research 2017, 25(1), 11-18. https://doi.org/10.3727/096504016X14685034103833

Abstract

Aristaless-like homeobox-4 (ALX4), a member of the Aristaless-like homeobox family, has been found to be involved in tumor cell proliferation, migration, and invasion. However, the role of ALX4 in hepatocellular carcinoma (HCC) remains largely unclear. Therefore, in this study we investigated the effects of ALX4 on HCC. The study results indicated that the expression of ALX4 was downregulated in HCC tissues and cell lines. Furthermore, we demonstrated that overexpression of ALX4 inhibited the proliferation, invasion, and epithelial–mesenchymal transition (EMT) in HCC cells. We also found that ALX4 had an inhibitory effect on the sonic hedgehog (Shh) signaling pathway. Taken together, the results suggest that ALX4 may be a promising target for HCC treatment.

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APA Style
Shi, Y., Sun, X., He, X. (2017). Overexpression of aristaless-like homeobox-4 inhibits proliferation, invasion, and EMT in hepatocellular carcinoma cells. Oncology Research, 25(1), 11-18. https://doi.org/10.3727/096504016X14685034103833
Vancouver Style
Shi Y, Sun X, He X. Overexpression of aristaless-like homeobox-4 inhibits proliferation, invasion, and EMT in hepatocellular carcinoma cells. Oncol Res. 2017;25(1):11-18 https://doi.org/10.3727/096504016X14685034103833
IEEE Style
Y. Shi, X. Sun, and X. He, “Overexpression of Aristaless-Like Homeobox-4 Inhibits Proliferation, Invasion, and EMT in Hepatocellular Carcinoma Cells,” Oncol. Res., vol. 25, no. 1, pp. 11-18, 2017. https://doi.org/10.3727/096504016X14685034103833



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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