ArticleOncotarget2015
HDAC9 promotes glioblastoma growth via TAZ-mediated EGFR pathway activation.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Unlocking glioblastoma: breakthroughs in molecular mechanisms and next-generation therapies.Medical oncology (Northwood, London, England) · 2025Pooled it
- SOX21 suppresses glioblastoma growth by repressing AP-1 activity.Cell death & disease · 2026Article
- Structure evaluation coupled with all-atom molecular dynamics and advanced quantum mechanical DFT revealed kaempferol as a potent binding flavonol for the epigenetic-target HDAC9.Journal of biosciences · 2026Article
- Targeting glioblastoma with HDAC inhibitors: insights into hydroxamic acid-based therapeutic strategies.Acta neuropathologica communications · 2025Article
- Thermal shift engagement assay for Class IIA histone deacetylase inhibitor screening.Results in chemistry · 2025Article
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- HDAC9 as a Privileged Target: Reviewing its Role in Different Diseases and Structure-activity Relationships (SARs) of its Inhibitors.Mini reviews in medicinal chemistry · 2024Review
- The Spectrum of Molecular Pathways in Gliomas-An Up-to-Date Review.Biomedicines · 2023Review
- The function of histone methylation and acetylation regulators in GBM pathophysiology.Frontiers in oncology · 2023Review
- A Selective Histone Deacetylase Inhibitor Induces Autophagy and Cell Death via SCNN1A Downregulation in Glioblastoma Cells.Cancers · 2022Article
- New locus underlying auriculocondylar syndrome (ARCND): 430 kb duplication involvingJournal of medical genetics · 2022Article
- Deoxyelephantopin Induces Apoptosis and Enhances Chemosensitivity of Colon Cancer via miR-205/Bcl2 Axis.International journal of molecular sciences · 2022Article
- HDAC9 Contributes to Serous Ovarian Cancer Progression through Regulating Epithelial-Mesenchymal Transition.Biomedicines · 2022Article
- Latest updates on cellular and molecular biomarkers of gliomas.Frontiers in oncology · 2022Review
- Genotoxic therapy and resistance mechanism in gliomas.Pharmacology & therapeutics · 2021Review
- Histone deacetylase (HDAC) 9: versatile biological functions and emerging roles in human cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- EGFR Activates a TAZ-Driven Oncogenic Program in Glioblastoma.Cancer research · 2021Article
- Quis Custodiet Ipsos Custodes (Who Controls the Controllers)? Two Decades of Studies on HDAC9.Life (Basel, Switzerland) · 2021Review
- Hippo Signaling Pathway in Gliomas.Cells · 2021Review
- MiR-365a-3p-Mediated Regulation of HELLS/GLUT1 Axis Suppresses Aerobic Glycolysis and Gastric Cancer Growth.Frontiers in oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.