Oncotarget

Research Papers:

The Hippo transducer TAZ promotes cell proliferation and tumor formation of glioblastoma cells through EGFR pathway

Rui Yang, Yanan Wu, Jiahua Zou, Ji Zhou, Mei Wang, Xiangwei Hao and Hongjuan Cui _

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Oncotarget. 2016; 7:36255-36265. https://doi.org/10.18632/oncotarget.9199

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Abstract

Rui Yang1,*, Yanan Wu1,*, Jiahua Zou1, Ji Zhou2, Mei Wang1, Xiangwei Hao3, Hongjuan Cui1

1State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China

2Department of Neurosurgery, Second Artillery General Hospital, Chinese People’s Liberation Army, Beijing 100088, China

3Chongqing Reproductive and Genentics Institute, Chongqing Obstetrics and Gynecology Hospital, Chongqing 400013, China

*These authors contributed equally to this work

Correspondence to:

Hongjuan Cui, email: [email protected], [email protected]

Keywords: TAZ, glioblastoma, cell proliferation, cell cycle, EGFR

Received: November 17, 2015     Accepted: April 16, 2016     Published: May 06, 2016

ABSTRACT

TAZ, a WW-domain-containing transcriptional co-activator, is important for development of various tissues in mammals. Recently, TAZ has been found to be overexpressed in some types of human cancers. However, the role of TAZ in glioblastoma remains unclear. In this study, we found that TAZ was overexpressed in prognostically poor glioblastoma patients. Through knocking down or overexpressing TAZ in U87 and LN229 cells, the expression level of TAZ was found to be positively related to cell proliferation in vitro and tumor formation in vivo. Further investigation indicated that TAZ could significantly promote the acceleration of cell cycle. Moreover, the western blot for p-EGFR, p-AKT, p-ERK1/2, p21, cyclin E and CDK2 proteins, target genes of the EGFR pathway, indicated that TAZ significantly activated EGFR/AKT/ERK signaling. Additionally, the blockage of EGFR pathway resulted in a significantly inhibition of cell proliferation induced by TAZ. Taken together, these results demonstrate that TAZ can promote proliferation and tumor formation in glioblastoma cells by potentiating the EGFR/AKT/ERK pathway, and provide the evidence for promising target for the treatment of glioblastoma.


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