HDAC9 promotes glioblastoma growth via TAZ-mediated EGFR pathway activation
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Rui Yang1, Yanan Wu1, Mei Wang1, Zhongfeng Sun1, Jiahua Zou1, Yundong Zhang2, Hongjuan Cui1
1State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, P.R. China
2Department of Neurosurgery, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, P.R. China
Yundong Zhang, e-mail: firstname.lastname@example.org
Keywords: HDAC9, TAZ, cell cycle, EGFR, Glioblastoma
Received: December 8, 2014 Accepted: January 26, 2015 Published: February 10, 2015
Histone deacetylase 9 (HDAC9), a member of class II HDACs, regulates a wide variety of normal and abnormal physiological functions. We found that HDAC9 is over-expressed in prognostically poor glioblastoma patients. Knockdown HDAC9 decreased proliferation in vitro and tumor formation in vivo. HDAC9 accelerated cell cycle in part by potentiating the EGFR signaling pathway. Also, HDAC9 interacted with TAZ, a key downstream effector of Hippo pathway. Knockdown of HDAC9 decreased the expression of TAZ. We found that overexpressed TAZ in HDAC9-knockdown cells abrogated the effects induced by HDAC9 silencing both in vitro and in vivo. We demonstrated that HDAC9 promotes tumor formation of glioblastoma via TAZ-mediated EGFR pathway activation, and provide the evidence for promising target for the treatment of glioblastoma.
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