IKBKE regulates cell proliferation and epithelial–mesenchymal transition of human malignant glioma via the Hippo pathway
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Jie Lu1,*, Yi Yang1,*, Gaochao Guo1, Yang Liu1, Zhimeng Zhang1, Shicai Dong1, Yang Nan1, Zhenyi Zhao2, Yue Zhong1 and Qiang Huang1
1Department of Neurosurgery, Tianjin Medical University General Hospital, Heping District, Tianjin 300052, China
2Department of Neurosurgery, Tianjin Baodi People's Hospital, Baodi District, Tianjin 301800, China
*These authors contributed equally to this work
Qiang Huang, email: firstname.lastname@example.org
Keywords: IKBKE, epithelial–mesenchymal transition (EMT), glioma, Hippo pathway
Received: October 12, 2016 Accepted: April 24, 2017 Published: May 10, 2017
IKBKE is increased in several types of cancers and is associated with tumour malignancy. In this study, we confirmed that IKBKE promoted glioma proliferation, migration and invasion in vitro. Then, we further discovered that IKBKE increased Yes-associated protein 1 (YAP1) and TEA domain family member 2 (TEAD2), two important Hippo pathway downstream factors, to induce an epithelial–mesenchymal transition (EMT), thus contributing to tumour invasion and metastasis. We also testified that YAP1 and TEAD2 promoted epithelial–mesenchymal transition (EMT) in malignant glioma. Furthermore, we constructed nude mouse subcutaneous and intracranial models to verify that IKBKE could attenuate U87-MG tumourigenicity in vivo. Collectively, our results suggest that IKBKE plays a pivotal role in regulating cell proliferation, invasion and epithelial–mesenchymal transition of malignant glioma cells in vitro and in vivo by impacting on the Hippo pathway. Therefore, targeting IKBKE may become a new strategy to treat malignant glioma.
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