ArticleBiology open2018
NGF reprograms metastatic melanoma to a bipotent glial-melanocyte neural crest-like precursor.
Article in Biology open, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- NGF-mediated tumor-stroma crosstalk promotes prostate cancer aggressiveness.Journal of translational medicine · 2026Article
- Evolution of Cancer Metastases via Lineage Trans-Differentiation.Research (Washington, D.C.) · 2026Article
- Optimal Control in Combination Therapy for Heterogeneous Cell Populations with Drug Synergies.Bulletin of mathematical biology · 2025Article
- A distinct pattern of growth and RAC1 signaling in melanoma brain metastasis cells.Neuro-oncology · 2023Article
- Nerve growth factor interacts with CHRM4 and promotes neuroendocrine differentiation of prostate cancer and castration resistance.Communications biology · 2021Article
- Defining the Hallmarks of Metastasis.Cancer research · 2019Review
- The convergent roles of CD271/p75 in neural crest-derived melanoma plasticity.Developmental biology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Melanoma pathogenesis from normal neural crest-derived melanocytes is often fatal due to aggressive cell invasion throughout the body. The identification of signals that reprogram de-differentiated, metastatic melanoma cells to a less aggressive and stable phenotype would provide a novel strategy to limit disease progression. In this study, we identify and test the function of developmental signals within the chick embryonic neural crest microenvironment to reprogram and sustain the transition of human metastatic melanoma to a neural crest cell-like phenotype. Results reveal that co-culture of the highly aggressive and metastatic human melanoma cell line C8161 upregulate a marker of melanosome formation (Mart-1) in the presence of embryonic day 3.5 chick trunk dorsal root ganglia. We identify nerve growth factor (NGF) as the signal within this tissue driving Mart-1 re-expression and show that NGF receptors trkA and p75 cooperate to induce Mart-1 re-expression. Furthermore, Mart-1 expressing C8161 cells acquire a gene signature of poorly aggressive C81-61 cells. These data suggest that targeting NGF signaling may yield a novel strategy to reprogram metastatic melanoma toward a benign cell type.
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Registered trials
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