ArticleThe Journal of pharmacology and experimental therapeutics2009
Abrogation of mitogen-activated protein kinase and Akt signaling by vandetanib synergistically potentiates histone deacetylase inhibitor-induced apoptosis in human glioma cells.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
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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.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
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- Nanodelivery Systems Targeting Epidermal Growth Factor Receptors for Glioma Management.Pharmaceutics · 2020Review
- Review
- Pre-clinical characterization of 4SC-202, a novel class I HDAC inhibitor, against colorectal cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- A MEK/PI3K/HDAC inhibitor combination therapy for KRAS mutant pancreatic cancer cells.Oncotarget · 2015Article
- Co-administration of ABT-737 and SAHA induces apoptosis, mediated by Noxa upregulation, Bax activation and mitochondrial dysfunction in PTEN-intact malignant human glioma cell lines.Journal of neuro-oncology · 2014Article
- Histone deacetylase inhibitors in glioblastoma: pre-clinical and clinical experience.Medical oncology (Northwood, London, England) · 2014Review
- Synergistic action by multi-targeting compounds produces a potent compound combination for human NSCLC both in vitro and in vivo.Cell death & disease · 2014Article
- Deregulated chromatin remodeling in the pathobiology of brain tumors.Neuromolecular medicine · 2013Review
- Bortezomib-induced sensitization of malignant human glioma cells to vorinostat-induced apoptosis depends on reactive oxygen species production, mitochondrial dysfunction, Noxa upregulation, Mcl-1 cleavage, and DNA damage.Molecular carcinogenesis · 2013Article
- New vandetanib analogs: fused tricyclic quinazolines with antiangiogenic potential.Investigational new drugs · 2012Article
- Histone deacetylase inhibitors: emerging mechanisms of resistance.Molecular pharmaceutics · 2011Review
- Bortezomib sensitizes malignant human glioma cells to TRAIL, mediated by inhibition of the NF-{kappa}B signaling pathway.Molecular cancer therapeutics · 2011Article
- Experimental approaches for the treatment of malignant gliomas.Pharmacology & therapeutics · 2010Review
- Targeting cellular pathways in glioblastoma multiforme.Signal transduction and targeted therapyReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Vandetanib is a multitargeted tyrosine kinase inhibitor. Our initial studies demonstrated that this agent blocks vascular endothelial growth factor receptor, epidermal growth factor receptor, and platelet-derived growth factor receptor phosphorylation and mitogen-activated protein kinase (MAPK)-mediated signaling in glioma cell lines in a dose-dependent manner. Despite these effects, we observed that vandetanib had little effect on apoptosis induction at clinically achievable concentrations. Because histone deacetylase inhibitors (HDACIs) have been suggested to regulate signaling protein transcription and downstream interactions via modulation of protein chaperone function through the 90-kDa heat shock protein, we investigated whether combining vandetanib with an HDACI could synergistically potentiate signaling pathway inhibition and apoptosis induction in a panel of malignant human glioma cell lines. Proliferation assays, apoptosis induction studies, and Western immunoblot analysis were conducted in cells treated with vandetanib and HDACIs as single agents or in combination. Vandetanib and suberoylanalide hydroxamic acid reduced proliferation in all cell lines when used as single agents, and the combination produced marked potentiation of growth inhibition as assessed by combinatorial methods. These effects were paralleled by potentiation of Akt signaling inhibition and apoptosis induction. Our results indicate that inhibition of histone deacetylation enhances the antiproliferative effect of vandetanib in malignant human glioma cell lines by enhancing inhibition of MAPK, Akt, and other downstream effectors that may have application in combinatorial therapeutics for these tumors.
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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.