HDAC9 promotes glioblastoma growth via TAZ-mediated EGFR pathway activation
作者： Rui Yang , Yanan Wu , Mei Wang , Zhongfeng Sun , Jiahua Zou
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摘要: Histone deacetylase 9 (HDAC9), a member of class II HDACs, regulates wide variety normal and abnormal physiological functions. We found that HDAC9 is over-expressed in prognostically poor glioblastoma patients. Knockdown decreased proliferation vitro tumor formation vivo. accelerated cell cycle part by potentiating the EGFR signaling pathway. Also, interacted with TAZ, key downstream effector Hippo expression TAZ. overexpressed TAZ HDAC9-knockdown cells abrogated effects induced silencing both demonstrated promotes via TAZ-mediated pathway activation, provide evidence for promising target treatment glioblastoma.
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