Research Papers:

FoxR2 promotes glioma proliferation by suppression of the p27 pathway

Xuejiao Liu, Ning Liu, Chenglong Yue, Dacheng Wang, Zhenglei Qi, Yiming Tu, Guokun Zhuang, Di Zhou, Shangfeng Gao, Mingshan Niu _ and Rutong Yu

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Oncotarget. 2017; 8:56255-56266. https://doi.org/10.18632/oncotarget.17447

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Xuejiao Liu1,2,*, Ning Liu1,4,*, Chenglong Yue1,*, Dacheng Wang1, Zhenglei Qi1, Yiming Tu1, Guokun Zhuang1, Di Zhou1, Shangfeng Gao1,2, Mingshan Niu3 and Rutong Yu1,2

1Insititute of Nervous System Diseases, Xuzhou Medical University, Xuzhou, Jiangsu, China

2Brain Hospital, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China

3Jiangsu Key Laboratory of Bone Marrow Stem Cell, Xuzhou Medical University, Xuzhou, Jiangsu, China

4Department of Neurosurgery, Huzhou Central Hospital, Huzhou, Zhejiang, China

*These authors contributed equally to this work

Correspondence to:

Mingshan Niu, email: [email protected]

Rutong Yu, email: [email protected]

Keywords: glioma, FoxR2, proliferation, migration, p27

Received: August 31, 2016     Accepted: April 14, 2017     Published: April 27, 2017


FoxR2 plays an important role in the development of many human tumors. However, the effects of FoxR2 on tumorigenicity of human glioma remain unclear. In this study, we investigated the roles of FoxR2 in cell proliferation and invasion of glioma. We found that overexpression of FoxR2 promoted the proliferation, migration and invasion of glioma cells. Knockout of FoxR2 induced G1 arrest by decreasing the expression levels of cyclin D1, cyclin E and p-Rb. Mechanistically, upregulation of FoxR2 increased the level and activity of MMP-2 and decreased the expression of p27. Furthermore, overexpression of FoxR2 decreased the nuclear accumulation of p27. Taken together, these results indicate that upregulation of FoxR2 may confer enhanced tumorigenicity in glioma cells.

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