ArticleScientific reports2018
Etoposide-resistance in a neuroblastoma model cell line is associated with 13q14.3 mono-allelic deletion and miRNA-15a/16-1 down-regulation.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Amphiphilic Semisynthetic Triterpenoids Impair Survival Pathways and Suppress Clonogenic Growth in Multidrug-Resistant High-Risk Neuroblastoma.International journal of molecular sciences · 2026Article
- Quaternary Phosphonium Salts Outperformed Vemurafenib (PLX) and Etoposide Against BRAFInternational journal of molecular sciences · 2026Article
- Design and Synthesis of New Coumarin Hybrids Active Against Drug-Sensitive and Drug-Resistant Neuroblastoma Cells.Antioxidants (Basel, Switzerland) · 2025Article
- From Early Diagnoses to New Treatments for Liver, Pancreatic, Gastric, and Colorectal Cancers Using Carbon Nanotubes: New Chances Still Underexplored.International journal of molecular sciences · 2025Review
- TPP-Based Nanovesicles Kill MDR Neuroblastoma Cells and Induce Moderate ROS Increase, While Exerting Low Toxicity Towards Primary Cell Cultures: An In Vitro Study.International journal of molecular sciences · 2025Article
- Detecting Telomeric DNA Damage by Immuno-Telo FISH.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Targeting NRAS via miR-1304-5p or farnesyltransferase inhibition confers sensitivity to ALK inhibitors in ALK-mutant neuroblastoma.Nature communications · 2024Article
- PTC596-Induced BMI-1 Inhibition Fights Neuroblastoma Multidrug Resistance by Inducing Ferroptosis.Antioxidants (Basel, Switzerland) · 2023Article
- Anti-CCL2 antibody combined with etoposide prolongs survival in a minimal residual disease mouse model of neuroblastoma.Scientific reports · 2023Article
- Therapy resistance in neuroblastoma: Mechanisms and reversal strategies.Frontiers in pharmacology · 2023Review
- Hormesis and Oxidative Distress: Pathophysiology of Reactive Oxygen Species and the Open Question of Antioxidant Modulation and Supplementation.Antioxidants (Basel, Switzerland) · 2022Review
- Antimicrobial Peptides and Cationic Nanoparticles: A Broad-Spectrum Weapon to Fight Multi-Drug Resistance Not Only in Bacteria.International journal of molecular sciences · 2022Review
- The role of ncRNAs in neuroblastoma: mechanisms, biomarkers and therapeutic targets.Biomarker research · 2022Review
- Oncopreventive and oncotherapeutic potential of licorice triterpenoid compound glycyrrhizin and its derivatives: Molecular insights.Pharmacological research · 2022Review
- Efficacy of High-Ozonide Oil in Prevention of Cancer Relapses Mechanisms and Clinical Evidence.Cancers · 2022Article
- Mutant p53Frontiers in genetics · 2022Article
- Single-cell transcriptomics of neuroblastoma identifies chemoresistance-associated genes and pathways.Computational and structural biotechnology journal · 2022Article
- Potential Role of miRNAs in the Acquisition of Chemoresistance in Neuroblastoma.Journal of personalized medicine · 2021Article
- Integrated Microarray to Identify the Hub miRNAs and Constructed miRNA-mRNA Network in Neuroblastoma Via Bioinformatics Analysis.Neurochemical research · 2021Article
- Downregulation of ATXN3 Enhances the Sensitivity to AKT Inhibitors (Perifosine or MK-2206), but Decreases the Sensitivity to Chemotherapeutic Drugs (Etoposide or Cisplatin) in Neuroblastoma Cells.Frontiers in oncology · 2021Article
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance is the major obstacle in successfully treating high-risk neuroblastoma. The aim of this study was to investigate the basis of etoposide-resistance in neuroblastoma. To this end, a MYCN-amplified neuroblastoma cell line (HTLA-230) was treated with increasing etoposide concentrations and an etoposide-resistant cell line (HTLA-ER) was obtained. HTLA-ER cells, following etoposide exposure, evaded apoptosis by altering Bax/Bcl2 ratio. While both cell populations shared a homozygous TP53 mutation encoding a partially-functioning protein, a mono-allelic deletion of 13q14.3 locus, where the P53 inducible miRNAs 15a/16-1 are located, and the consequent miRNA down-regulation were detected only in HTLA-ER cells. This event correlated with BMI-1 oncoprotein up-regulation which caused a decrease in p16 tumor suppressor content and a metabolic adaptation of HTLA-ER cells. These results, taken collectively, highlight the role of miRNAs 15a/16-1 as markers of chemoresistance.
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