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

被引:26
|
作者
Yang, Rui [1 ]
Wu, Yanan [1 ]
Zou, Jiahua [1 ]
Zhou, Ji [2 ]
Wang, Mei [1 ]
Hao, Xiangwei [3 ]
Cui, Hongjuan [1 ]
机构
[1] Southwest Univ, State key Lab Silkworm Genome Biol, Chongqing 400715, Peoples R China
[2] Chinese Peoples Liberat Army, Artillery Gen Hosp 2, Dept Neurosurg, Beijing 100088, Peoples R China
[3] Chongqing Obstet & Gynecol Hosp, Chongqing Reprod & Genent Inst, Chongqing 400013, Peoples R China
来源
ONCOTARGET | 2016年 / 7卷 / 24期
基金
高等学校博士学科点专项科研基金;
关键词
TAZ; glioblastoma; cell proliferation; cell cycle; EGFR; GROWTH-FACTOR RECEPTOR; SIGNALING PATHWAY; CANCER CELLS; COACTIVATOR; GLIOMAS; TUMORIGENICITY; ACTIVATION; EXPRESSION; ONCOGENE;
D O I
10.18632/oncotarget.9199
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:36255 / 36265
页数:11
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