ArticlePloS one2012
Galectin-3 impairment of MYCN-dependent apoptosis-sensitive phenotype is antagonized by nutlin-3 in neuroblastoma cells.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- SGSS05-NS3, a covalent SETD8 inhibitor that activates p53 pathway in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Targeting the MYCN-MDM2 pathways for cancer therapy: Are they druggable?Genes & diseases · 2025Review
- Galectin inhibitors and nanoparticles as a novel therapeutic strategy for glioblastoma multiforme.American journal of cancer research · 2024Review
- Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy.Biomarker research · 2023Review
- LIN28B inhibition sensitizes cells to p53-restoring PPI therapy through unleashed translational suppression.Oncogenesis · 2022Article
- Venetoclax-based Rational Combinations are Effective in Models ofMolecular cancer therapeutics · 2021Article
- Targeting the p53-MDM2 pathway for neuroblastoma therapy: Rays of hope.Cancer letters · 2021Review
- Sweetening the hallmarks of cancer: Galectins as multifunctional mediators of tumor progression.The Journal of experimental medicine · 2020Review
- MRE11 inhibition highlights a replication stress-dependent vulnerability of MYCN-driven tumors.Cell death & disease · 2018Article
- TrkB-Target Galectin-1 Impairs Immune Activation and Radiation Responses in Neuroblastoma: Implications for Tumour Therapy.International journal of molecular sciences · 2018Review
- Galectin-3: One Molecule for an Alphabet of Diseases, from A to Z.International journal of molecular sciences · 2018Review
- Galectin Targeted Therapy in Oncology: Current Knowledge and Perspectives.International journal of molecular sciences · 2018Review
- PARP inhibitors enhance replication stress and cause mitotic catastrophe in MYCN-dependent neuroblastoma.Oncogene · 2017Article
- Combination of galectin inhibitor GCS-100 and BH3 mimetics eliminates both p53 wild type and p53 null AML cells.Biochimica et biophysica acta · 2016Article
- Exploitation of the Apoptosis-Primed State of MYCN-Amplified Neuroblastoma to Develop a Potent and Specific Targeted Therapy Combination.Cancer cell · 2016Article
- The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress.Cell death and differentiation · 2016Article
- Intelectin 1 suppresses the growth, invasion and metastasis of neuroblastoma cells through up-regulation of N-myc downstream regulated gene 2.Molecular cancer · 2015Article
- Galectin-3 is a marker of favorable prognosis and a biologically relevant molecule in neuroblastic tumors.Cell death & disease · 2014Article
- MYCN-mediated transcriptional repression in neuroblastoma: the other side of the coin.Frontiers in oncology · 2013Article
- Molecular mechanisms of MYCN-dependent apoptosis and the MDM2-p53 pathway: an Achille's heel to be exploited for the therapy of MYCN-amplified neuroblastoma.Frontiers in oncology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neuroblastoma. We recently reported that the apoptosis-sensitive phenotype induced by MYCN is linked to stabilization of p53 and its proapoptotic kinase HIPK2. In MYCN primed neuroblastoma cells, further activation of both HIPK2 and p53 by Nutlin-3 leads to massive apoptosis in vitro and to tumor shrinkage and impairment of metastasis in xenograft models. Here we report that Galectin-3 impairs MYCN-primed and HIPK2-p53-dependent apoptosis in neuroblastoma cells. Galectin-3 is broadly expressed in human neuroblastoma cell lines and tumors and is repressed by MYCN to induce the apoptosis-sensitive phenotype. Despite its reduced levels, Galectin-3 can still exert residual antiapoptotic effects in MYCN amplified neuroblastoma cells, possibly due to its specific subcellular localization. Importantly, Nutlin-3 represses Galectin-3 expression, and this is required for its potent cell killing effect on MYCN amplified cell lines. Our data further characterize the apoptosis-sensitive phenotype induced by MYCN, expand our understanding of the activity of MDM2-p53 antagonists and highlight Galectin-3 as a potential biomarker for the tailored p53 reactivation therapy in patients with high-risk neuroblastomas.
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