Oncotarget

Research Papers:

Trefoil factor 3 contributes to the malignancy of glioma via regulating HIF-1α

Shuo Diao, Qianqian Zheng, Jian Gao, Yiqun Yao, Siyang Ren, Yongjian Liu and Yinghui Xu _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:76770-76782. https://doi.org/10.18632/oncotarget.20010

Metrics: PDF 1298 views  |   HTML 1910 views  |   ?  


Abstract

Shuo Diao1, Qianqian Zheng2, Jian Gao3, Yiqun Yao1, Siyang Ren1, Yongjian Liu4 and Yinghui Xu1

1Department of Neurosurgery, First Affiliated Hospital, Dalian Medical University, Dalian, People’s Republic of China

2Department of Pathophysiology, Basic Medical College, China Medical University, Shenyang, People’s Republic of China

3Center of Laboratory Technology and Experimental Medicine, China Medical University, Shenyang, People’s Republic of China

4Department of Interventional Therapy, First Affiliated Hospital, Dalian Medical University, Dalian, People’s Republic of China

Correspondence to:

Yinghui Xu, email: [email protected]

Keywords: TFF3, glioblastoma, HIF-1α, proliferation, apoptosis

Received: March 14, 2017    Accepted: June 27, 2017    Published: August 07, 2017

ABSTRACT

Trefoil factor 3 (TFF3) plays significant roles in several solid tumors. However, the expression pattern and function of TFF3 in glioblastoma (GBM) have not been reported. Here, we report that expression level of TFF3 significantly elevated in glioma and correlated with the prognosis of glioma patients. Then we found TFF3 promotes proliferation, invasion, and migration and inhibits apoptosis of glioma cells in vitro, and delayed tumor progression in subcutaneous xenograft nude mice, and prolonged the median survival time in orthotopic xenograft mice. Moreover, knockdown of TFF3 reduced the expression of HIF-1α through a hypoxia-independent manner. These findings suggest that targeting TFF3 may offer a novel strategy for therapeutic intervention of malignant gliomas.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 20010