ArticleScientific reports2015
Inhibition of hypoxia inducible factors combined with all-trans retinoic acid treatment enhances glial transdifferentiation of neuroblastoma cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Review
- The Hypoxia-Retinoid Axis in Idiopathic Pulmonary Fibrosis: Multifaceted Etiology and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Mitoribosomal synthetic lethality overcomes multidrug resistance in MYC-driven neuroblastoma.Cell death & disease · 2023Article
- FGFR1 is a potential therapeutic target in neuroblastoma.Cancer cell international · 2022Article
- Hypoxia-Inducible Factor-1α (HIF-1α) Inhibition Impairs Retinoic Acid-Induced Differentiation in SH-SY5Y Neuroblastoma Cells, Leading to Reduced Neurite Length and Diminished Gene Expression Related to Cell Differentiation.Neurochemical research · 2022Article
- Mechanisms involved in selecting and maintaining neuroblastoma cancer stem cell populations, and perspectives for therapeutic targeting.World journal of stem cells · 2021Review
- Perspective on Similarities and Possible Overlaps of Congenital Disease Formation-Exemplified on a Case of Congenital Diaphragmatic Hernia and Neuroblastoma in a Neonate.Children (Basel, Switzerland) · 2021Article
- AQP1-Driven Migration Is Independent of Other Known Adverse Factors but Requires a Hypoxic Undifferentiated Cell Profile in Neuroblastoma.Children (Basel, Switzerland) · 2021Article
- An overview of neuroblastoma cell lineage phenotypes andExperimental biology and medicine (Maywood, N.J.) · 2020Review
- Functional characterization of full-length BARD1 strengthens its role as a tumor suppressor in neuroblastoma.Journal of Cancer · 2020Article
- Hypoxia in the Initiation and Progression of Neuroblastoma Tumours.International journal of molecular sciences · 2019Review
- HIF-1 transcription activity: HIF1A driven response in normoxia and in hypoxia.BMC medical genetics · 2019Article
- Cancer Stem Cells in Neuroblastoma: Expanding the Therapeutic Frontier.Frontiers in molecular neuroscience · 2019Review
- Collaborative ISL1/GATA3 interaction in controlling neuroblastoma oncogenic pathways overlapping with but distinct from MYCN.Theranostics · 2019Article
- Fine mapping of 2q35 high-risk neuroblastoma locus reveals independent functional risk variants and suggests full-length BARD1 as tumor-suppressor.International journal of cancer · 2018Article
- WNT signaling, the development of the sympathoadrenal-paraganglionic system and neuroblastoma.Cellular and molecular life sciences : CMLS · 2018Review
- Lysine-specific demethylase LSD1 regulates autophagy in neuroblastoma through SESN2-dependent pathway.Oncogene · 2017Article
- 3D collagen architecture induces a conserved migratory and transcriptional response linked to vasculogenic mimicry.Nature communications · 2017Article
- Combined epigenetic and differentiation-based treatment inhibits neuroblastoma tumor growth and links HIF2α to tumor suppression.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma (NBL) is a heterogeneous tumor characterized by a wide range of clinical manifestations. A high tumor cell differentiation grade correlates to a favorable stage and positive outcome. Expression of the hypoxia inducible factors HIF1-α (HIF1A gene) and HIF2-α (EPAS1 gene) and/or hypoxia-regulated pathways has been shown to promote the undifferentiated phenotype of NBL cells. Our hypothesis is that HIF1A and EPAS1 expression represent one of the mechanisms responsible for the lack of responsiveness of NBL to differentiation therapy. Clinically, high levels of HIF1A and EPAS1 expression were associated with inferior survival in two NBL microarray datasets, and patient subgroups with lower expression of HIF1A and EPAS1 showed significant enrichment of pathways related to neuronal differentiation. In NBL cell lines, the combination of all-trans retinoic acid (ATRA) with HIF1A or EPAS1 silencing led to an acquired glial-cell phenotype and enhanced expression of glial-cell differentiation markers. Furthermore, HIF1A or EPAS1 silencing might promote cell senescence independent of ATRA treatment. Taken together, our data suggest that HIF inhibition coupled with ATRA treatment promotes differentiation into a more benign phenotype and cell senescence in vitro. These findings open the way for additional lines of attack in the treatment of NBL minimal residue disease.
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