ArticleNature communications2017
low neurotrophin receptor CD271 regulates phenotype switching in melanoma.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 82 citations in OpenAlex.
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- Trametinib-Resistant Melanoma Cells Displaying MITFInternational journal of molecular sciences · 2023Article
- Reactive Oxygen Species Regulation of Chemoresistance and Metastatic Capacity of Melanoma: Role of the Cancer Stem Cell Marker CD271.Biomedicines · 2023Article
- A Comprehensive Analysis of Cutaneous Melanoma Patients in Greece Based on Multi-Omic Data.Cancers · 2023Article
- Escape from NK cell tumor surveillance by NGFR-induced lipid remodeling in melanoma.Science advances · 2023Article
- Cholinergic neurodegeneration and cholesterol metabolism dysregulation by constitutive p75Frontiers in molecular neuroscience · 2023Article
- p53 Family in Resistance to Targeted Therapy of Melanoma.International journal of molecular sciences · 2022Review
- New Insights into the Phenotype Switching of Melanoma.Cancers · 2022Review
- Decoding molecular programs in melanoma brain metastases.Nature communications · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cutaneous melanoma represents the most fatal skin cancer due to its high metastatic capacity. According to the "phenotype switching" model, the aggressive nature of melanoma cells results from their intrinsic potential to dynamically switch from a high-proliferative/low-invasive to a low-proliferative/high-invasive state. Here we identify the low affinity neurotrophin receptor CD271 as a key effector of phenotype switching in melanoma. CD271 plays a dual role in this process by decreasing proliferation, while simultaneously promoting invasiveness. Dynamic modification of CD271 expression allows tumor cells to grow at low levels of CD271, to reduce growth and invade when CD271 expression is high, and to re-expand at a distant site upon decrease of CD271 expression. Mechanistically, the cleaved intracellular domain of CD271 controls proliferation, while the interaction of CD271 with the neurotrophin receptor Trk-A modulates cell adhesiveness through dynamic regulation of a set of cholesterol synthesis genes relevant for patient survival.
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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.