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Knockdown of Rap2B Inhibits the Proliferation and Invasion in Hepatocellular Carcinoma Cells

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* Department of Gastroenterology and Hepatology, Chinese PLA General Hospital, Beijing, P.R. China
† Emergency Department, Shanxi Provincial People’s Hospital, Taiyuan, P.R. China

Oncology Research 2017, 25(1), 19-27. https://doi.org/10.3727/096504016X14685034103914

Abstract

Rap2B, a member of the Ras family of small GTP-binding proteins, was found to be highly expressed in various human tumors and plays an important role in the development of tumors. However, the function of Rap2B in hepatocellular carcinoma (HCC) remains unclear. Therefore, in this study, we investigated the biological functions of Rap2B in HCC and the potential underlying mechanisms. Our results indicated that Rap2B was highly expressed in HCC tissues and cell lines. Rap2B silencing obviously inhibited the proliferation, migration, and invasion of HCC cells, as well as attenuated xenografted tumor growth in vivo. Furthermore, Rap2B silencing greatly reduced the expression levels of phosphorylated focal adhesion kinase (p-FAK), matrix metalloproteinase-2 (MMP-2), and MMP-9 in HCC cells. In conclusion, our data suggest that Rap2B silencing inhibits the proliferation and invasion in HCC cells. Thus, Rap2B may have potential as a treatment for HCC.

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APA Style
Zhang, L., Duan, H., Yang, Y. (2017). Knockdown of rap2b inhibits the proliferation and invasion in hepatocellular carcinoma cells. Oncology Research, 25(1), 19-27. https://doi.org/10.3727/096504016X14685034103914
Vancouver Style
Zhang L, Duan H, Yang Y. Knockdown of rap2b inhibits the proliferation and invasion in hepatocellular carcinoma cells. Oncol Res. 2017;25(1):19-27 https://doi.org/10.3727/096504016X14685034103914
IEEE Style
L. Zhang, H. Duan, and Y. Yang, “Knockdown of Rap2B Inhibits the Proliferation and Invasion in Hepatocellular Carcinoma Cells,” Oncol. Res., vol. 25, no. 1, pp. 19-27, 2017. https://doi.org/10.3727/096504016X14685034103914



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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