ArticleJournal of experimental & clinical cancer research : CR2015
Targeted inhibition of MEK1 by cobimetinib leads to differentiation and apoptosis in neuroblastoma cells.
Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Targeting the MEK/ERK Pathway to Suppress P-Glycoprotein and Reverse Carfilzomib Resistance in Multiple Myeloma.International journal of molecular sciences · 2025Article
- Emerging Trends in Neuroblastoma Diagnosis, Therapeutics, and Research.Molecular neurobiology · 2025Review
- Large-scale control over collective cell migration using light-activated epidermal growth factor receptors.Cell systems · 2025Article
- Preclinical Therapeutic Efficacy of RAF/MEK/ERK and IGF1R/AKT/mTOR Inhibition in Neuroblastoma.Cancers · 2024Article
- The Effects of FABP4 on Cardiovascular Disease in the Aging Population.Current atherosclerosis reports · 2024Review
- Trametinib activates endogenous neurogenesis and recovers neuropathology in a model of Alzheimer's disease.Experimental & molecular medicine · 2023Article
- Identifying Potential Molecular Targets in Fungi Based on (Dis)Similarities in Binding Site Architecture with Proteins of the Human Pharmacolome.Molecules (Basel, Switzerland) · 2023Article
- Discovery of Cobimetinib as a novel A-FABP inhibitor using machine learning and molecular docking-based virtual screening.RSC advances · 2022Article
- Synthetic Heterocyclic Derivatives as Kinase Inhibitors Tested for the Treatment of Neuroblastoma.Molecules (Basel, Switzerland) · 2021Review
- Targeting RAS in pediatric cancer: is it becoming a reality?Current opinion in pediatrics · 2020Review
- Article
- Dual-Specificity Phosphatases in Neuroblastoma Cell Growth and Differentiation.International journal of molecular sciences · 2019Review
- SYK Inhibition Potentiates the Effect of Chemotherapeutic Drugs on Neuroblastoma Cells in Vitro.Cancers · 2019Article
- Expression of TLR4 gene is downregulated in acquired immune deficiency syndrome-associated Kaposi's sarcoma.Experimental and therapeutic medicine · 2019Article
- Inhibition of chemerin/CMKLR1 axis in neuroblastoma cells reduces clonogenicity and cell viabilityOncotarget · 2017Article
- Nerve growth factor: role in growth, differentiation and controlling cancer cell development.Journal of experimental & clinical cancer research : CR · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuroblastoma (NB) is one of the most common childhood malignancies. Currently, high risk NB carries a poor outcome and significant treatment related toxicities and, thus has been a focus for new therapeutics research in pediatric oncology. In this study, we evaluated the effects of the MEK inhibitor cobimetinib, as a single agent and in combinations, on the growth, survival and differentiation properties against a molecularly representative panel of NB cell lines.
methodsIn vitro anti-proliferative activity of cobimetinib alone or in combination was investigated by cell viability assays and its target modulatory activity was evaluated using phospho-kinases antibody arrays and western blot analysis. To determine the effect of combination with cis-RA on differentiation and resulting enhanced cellular cytotoxicity, the expression of glial fibrillary acidic protein (GFAP) and microtubule-associated protein 2 (MAP2) expression levels were examined by immuno-fluorescence.
resultsOur findings show that cobimetinib alone induced a concentration-dependent loss of cell viability in all NB cell lines. In addition, cobimetinib showed feedback activation of MEK1/2, and the dephosphorylation of extracellular signal-regulated kinases (ERK1/2) and c-RAF, providing information on the biological correlates of MEK inhibition in NB. Combined treatment with cis-RA, led to differentiation and enhanced sensitization of NB cells lines to cobimetinib.
conclusionCollectively, our results provide evidence that cobimetinib, in combination with cis-RA, represents a feasible option to develop novel treatment strategies for refractory NB.
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