ArticleCell death and differentiation2009
Interfering with multimerization of netrin-1 receptors triggers tumor cell death.
Article in Cell death and differentiation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Netrin-1-CD146 and netrin-1-S100A9 are associated with early stage of lymph node metastasis in colorectal cancer.BMC gastroenterology · 2024Article
- Role of Receptors in Relation to Plaques and Tangles in Alzheimer's Disease Pathology.International journal of molecular sciences · 2021Review
- Dependence receptors: new targets for cancer therapy.EMBO molecular medicine · 2021Review
- Δ40p53 isoform up-regulates netrin-1/UNC5B expression and potentiates netrin-1 pro-oncogenic activity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- A ligand-insensitive UNC5B splicing isoform regulates angiogenesis by promoting apoptosis.Nature communications · 2021Article
- Article
- The Ectodysplasin receptor EDAR acts as a tumor suppressor in melanoma by conditionally inducing cell death.Cell death and differentiation · 2019Article
- Kremen1-induced cell death is regulated by homo- and heterodimerization.Cell death discovery · 2019Article
- Revisiting Netrin-1: One Who Guides (Axons).Frontiers in cellular neuroscience · 2018Review
- DCC mutation update: Congenital mirror movements, isolated agenesis of the corpus callosum, and developmental split brain syndrome.Human mutation · 2018Review
- TRIM9-dependent ubiquitination of DCC constrains kinase signaling, exocytosis, and axon branching.Molecular biology of the cell · 2017Article
- TIA1 is a gender-specific disease modifier of a mild mouse model of spinal muscular atrophy.Scientific reports · 2017Article
- Epidermal Growth Factor Receptor-Dependent Mutual Amplification between Netrin-1 and the Hepatitis C Virus.PLoS biology · 2016Article
- Microarray Expression Data Identify DCC as a Candidate Gene for Early Meningioma Progression.PloS one · 2016Article
- Peptides derived from the dependence receptor ALK are proapoptotic for ALK-positive tumors.Cell death & disease · 2015Article
- Netrin-1 promoted pancreatic cancer cell proliferation by upregulation of Mdm2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- The crystal structure of netrin-1 in complex with DCC reveals the bifunctionality of netrin-1 as a guidance cue.Neuron · 2014Article
- Neural migration. Structures of netrin-1 bound to two receptors provide insight into its axon guidance mechanism.Science (New York, N.Y.) · 2014Article
- Netrin-1 expression is an independent prognostic factor for poor patient survival in brain metastases.PloS one · 2014Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Netrin-1 was recently proposed to control tumorigenesis by inhibiting apoptosis induced by the dependence receptors DCC (Deleted in colorectal cancer) and UNC5H. Although the loss of these dependence receptors' expression has been described as a selective advantage for tumor growth and progression in numerous cancers, recent observations have shown that some tumors may use an alternative strategy to block dependence receptor-induced programmed cell death: the autocrine expression of netrin-1. This alternative strategy has been observed in a large fraction of aggressive breast cancers, neuroblastoma, pancreatic adenocarcinoma, and lung cancer. This observation is of potential interest regarding future targeted therapy, as in such cases interfering with the ability of netrin-1 to inhibit DCC or UNC5H-induced cell death is associated with apoptosis of netrin-1-expressing tumor cells in vitro, and with inhibition of tumor growth or metastasis in different animal tumor models. The understanding of the mechanism by which netrin-1 inhibits cell death is therefore of interest. Here, we show that netrin-1 triggers the multimerization of both DCC and UNC5H2 receptors, and that multimerization of the intracellular domain of DCC and UNC5H2 is the critical step to inhibit the proapoptotic effects of both of these receptors. Taking advantage of this property, we utilized a recombinant specific domain of DCC that (i) interacts with netrin-1 and (ii) inhibits netrin-1-induced multimerization, to trigger apoptosis in netrin-dependent tumor cells.
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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.