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GGNBP2 Suppresses the Proliferation, Invasion, and Migration of Human Glioma Cells

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* Department of Neurosurgery, The People’s Hospital of Leshan City, Leshan, Sichuan, P.R. China
† Department of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Yuzhong, Chongqing, P.R. China

Oncology Research 2017, 25(5), 831-842. https://doi.org/10.3727/096504016X14816726393937

Abstract

Gliomas are the most common and aggressive type of primary adult brain tumors. Although GGNBP2 has previously been considered to be a tumor suppressor gene, little is known about the association between GGNBP2 and glioma. In this study, we clearly demonstrated that GGNBP2 was downexpressed in glioma tissues, and its downexpression is related to the pathological grade and overall survival of patients with gliomas. Overexpression of GGNBP2 suppressed the proliferation, migration, and invasion of glioma cells. Mechanistically, we demonstrated that the PI3K/Akt and Wnt/β-catenin signaling pathways were suppressed by GGNBP2 overexpression. In contrast, knockdown of GGNBP2 has precisely the opposite effect. Collectively, these data indicate that GGNBP2 shows tumor suppressive activity in human glioma cells and may stand out as a potential therapeutic target for glioma.

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APA Style
Zhan, A., Lei, B., Wu, H., Wen, Y., Zheng, L. et al. (2017). GGNBP2 suppresses the proliferation, invasion, and migration of human glioma cells. Oncology Research, 25(5), 831-842. https://doi.org/10.3727/096504016X14816726393937
Vancouver Style
Zhan A, Lei B, Wu H, Wen Y, Zheng L, Wang S, et al. GGNBP2 suppresses the proliferation, invasion, and migration of human glioma cells. Oncol Res. 2017;25(5):831-842 https://doi.org/10.3727/096504016X14816726393937
IEEE Style
A. Zhan et al., “GGNBP2 Suppresses the Proliferation, Invasion, and Migration of Human Glioma Cells,” Oncol. Res., vol. 25, no. 5, pp. 831-842, 2017. https://doi.org/10.3727/096504016X14816726393937



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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