Dependence receptors: a new paradigm in cell signaling and cancer therapy
Open accessAbstract
Dependence receptors (DRs) now form a family of more than a dozen membrane receptors that are not linked by their structure, but by common functional traits. The most notable is their ability to trigger two opposite signaling pathways: in the presence of ligand, these receptors activate classic signaling pathways implicated in cell survival, migration and differentiation. In the absence of ligand, they do not stay inactive, rather they elicit an apoptotic signal. Thus, cells expressing this kind of receptor are dependent on the presence of ligand in the extracellular environment to survive. This review will recapitulate the increasing data regarding the molecular mechanisms associated with DRs, their potential implication during development, as well as their deregulation during tumorigenesis and, finally, their emergence as new possible therapeutic targets for cancer treatment.
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The senolytic transcripts included EFNB1, EFNB3, p21, PAI-2, PI3KCD, and BCL-xL.
“the senolytic transcripts included components of ephrin survival-regulating dependence receptor mechanisms (Goldschneider & Mehlen, 2010), ephrin ligand (EFN) B1, and EFNB3, as well as the cyclin-dependent kinase inhibitor 1A (p21), plasminogen-activated inhibitor-2 (PAI-2)”
From The Achilles' heel of senescent cells: from transcriptome to senolytic drugs (2015) · cites this paper as Goldschneider & Mehlen, 2010
Family of dependence receptors consists of approximately 20 members, including NTN1 receptors DCC, UNC5A-D, NTRK3, and PTCH1.
“The family of dependence receptors consists of approximately 20 members, including: (1) the netrin 1 (NTN1) receptors DCC netrin 1 receptor (DCC), unc-5 netrin receptor A (UNC5A), UNC5B, UNC5C, and UNC5D; (2) the neurotrophin receptor neurotrophic receptor tyrosine kinase 3 (NTRK3); and (3) the sonic hedgehog (SHH) receptor patched 1 (PTCH1) [267, 349, 350].”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [349]
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Self-citationThe Patched dependence receptor triggers apoptosis through a DRAL–caspase-9 complex
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“Interestingly, the senolytic transcripts included components of ephrin survival-regulating dependence receptor mechanisms (Goldschneider & Mehlen, 2010), ephrin ligand (EFN) B1, and EFNB3, as well as the cyclin-dependent kinase inhibitor 1A (p21), plasminogen-activated inhibitor-2 (PAI-2), the…”
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- Authors
- Goldschneider, D., & Mehlen, P.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Mehlen, P
- ORCID
- Mehlen, P
- Venue
- Oncogene
- Published
- 2010-02-22
- Volume
- 29
- Issue
- 13
- Pages
- 1865-1882
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W1984743597
- Cited by
- 169
- References
- 7
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 4 · 2023: 4 · 2022: 8 · 2021: 12 · 2020: 11 · 2019: 9 · 2018: 14 · 2017: 12 · 2016: 10 · 2015: 10 · 2014: 14 · 2013: 15 · 2012: 11
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oncogene (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- dependence receptors, ligand-dependent signaling, apoptosis, cell survival signaling, cell migration, cell differentiation, carcinogenesis, cancer therapy, therapeutic target, development (biology)
- MeSH terms
- Animals, Cell Differentiation, Cell Movement, Cell Survival, Cell Transformation, Neoplastic, Ligands, Neoplasms, Signal Transduction, Drug Delivery Systems, Apoptosis, Phosphatidylinositol 3-Kinases, Tumor Suppressor Proteins, Cell Line, Tumor, Extracellular Signal-Regulated MAP Kinases, TNF-Related Apoptosis-Inducing Ligand, ErbB Receptors
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