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Empty Spiracles Homeobox 2 (EMX2) Inhibits the Invasion and Tumorigenesis in Colorectal Cancer Cells

Yan Zhang, Gang Cao, Qing-gong Yuan, Jun-hui Li, Wen-Bin Yang

Department of General Surgery, The Second Affiliated Hospital of Medical School, Xi’an Jiaotong University, Xi’an, P.R. China

Oncology Research 2017, 25(4), 537-544. https://doi.org/10.3727/096504016X14756640150695

Abstract

Empty spiracles homeobox 2 (EMX2) is a homeodomain-containing transcription factor that plays an essential role in tumorigenesis. However, to the best of our knowledge, the role of EMX2 in human colorectal cancer (CRC) is still unclear. Thus, the aim of this study was to investigate the expression and role of EMX2 in CRC. Our results demonstrated that the expression of EMX2 was greatly decreased in CRC tissues and cell lines. Overexpression of EMX2 significantly inhibited the proliferation in vitro and CRC tumor growth in nude mice. In addition, EMX2 also inhibited the migration and invasion of CRC cells. Mechanically, overexpression of EMX2 downregulated the expression levels of β-catenin, cyclin D1, and c-Myc in CRC cells. Taken together, our study demonstrates that EMX2 inhibits proliferation and tumorigenesis through inactivation of the Wnt/β-catenin pathway in CRC cells. Therefore, EMX2 may be a potential therapeutic target for the treatment of CRC.

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APA Style
Zhang, Y., Cao, G., Yuan, Q., Li, J., Yang, W. (2017). Empty spiracles homeobox 2 (EMX2) inhibits the invasion and tumorigenesis in colorectal cancer cells. Oncology Research, 25(4), 537-544. https://doi.org/10.3727/096504016X14756640150695
Vancouver Style
Zhang Y, Cao G, Yuan Q, Li J, Yang W. Empty spiracles homeobox 2 (EMX2) inhibits the invasion and tumorigenesis in colorectal cancer cells. Oncol Res. 2017;25(4):537-544 https://doi.org/10.3727/096504016X14756640150695
IEEE Style
Y. Zhang, G. Cao, Q. Yuan, J. Li, and W. Yang "Empty Spiracles Homeobox 2 (EMX2) Inhibits the Invasion and Tumorigenesis in Colorectal Cancer Cells," Oncol. Res., vol. 25, no. 4, pp. 537-544. 2017. https://doi.org/10.3727/096504016X14756640150695



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