title: HDAC9 promotes glioblastoma growth via TAZ-mediated EGFR pathway activation.
abstract: 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.
authors.affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, P.R. China.
authors.forename: Rui
authors.initials: R
authors.lastname: Yang
authors.affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, P.R. China.
authors.forename: Yanan
authors.initials: Y
authors.lastname: Wu
authors.affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, P.R. China.
authors.forename: Mei
authors.initials: M
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, P.R. China.
authors.forename: Zhongfeng
authors.initials: Z
authors.lastname: Sun
authors.affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, P.R. China.
authors.forename: Jiahua
authors.initials: J
authors.lastname: Zou
authors.affiliation: Department of Neurosurgery, Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, P.R. China.
authors.forename: Yundong
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, P.R. China.
authors.forename: Hongjuan
authors.initials: H
authors.lastname: Cui
mesh_terms: D000818:Animals; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000502:physiology; D066246:ErbB Receptors / Q000378:metabolism*; D005260:Female; D005909:Glioblastoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D064593:Heterografts; D006655:Histone Deacetylases / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism*; D051379:Mice; D016513:Mice, SCID; D011379:Prognosis; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D015534:Trans-Activators; D014157:Transcription Factors; D000091364:Transcriptional Coactivator with PDZ-Binding Motif Proteins; D023041:Xenograft Model Antitumor Assays
chemical_list: D047908:Intracellular Signaling Peptides and Proteins; D012097:Repressor Proteins; D015534:Trans-Activators; D014157:Transcription Factors; D000091364:Transcriptional Coactivator with PDZ-Binding Motif Proteins; C551991:WWTR1 protein, human; C512478:EGFR protein, human; D066246:ErbB Receptors; C486544:HDAC9 protein, human; D006655:Histone Deacetylases
keywords: EGFR; HDAC9; TAZ; cell cycle; glioblastoma