ArticleThe Journal of experimental medicine2017
The epidermal polarity protein Par3 is a non-cell autonomous suppressor of malignant melanoma.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Article
- Atypical E-cadherin attachments mediate melanoblast migration through confined epithelial spaces.The Journal of cell biology · 2026Article
- Melanocyte differentiation and mechanosensation are differentially modulated by distinct extracellular matrix proteins.EMBO reports · 2025Article
- Review
- Dihydroartemisinin inhibits melanoma migration and metastasis by affecting angiogenesis.Phytotherapy research : PTR · 2025Article
- Unveiling the potential of biomechanics in pioneering innovative strategies for cancer therapy.Theranostics · 2025Review
- Dangerous liaisons: Loss of keratinocyte control over melanocytes in melanomagenesis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Contribution of Keratinocytes in Skin Cancer Initiation and Progression.International journal of molecular sciences · 2024Review
- Melanoma cells repress Desmoglein 1 in keratinocytes to promote tumor cell migration.The Journal of cell biology · 2023Article
- Persistent cell contacts enable E-cadherin/HMR-1- and PAR-3-based symmetry breaking within a developing C. elegans epithelium.Developmental cell · 2023Article
- GABA Regulates Electrical Activity and Tumor Initiation in Melanoma.Cancer discovery · 2023Article
- E-Cadherin Is Expressed in Epithelial Cells of the Choroid Plexus in Human and Mouse Brains.Current issues in molecular biology · 2023Article
- Matriptase-dependent epidermal pre-neoplasm in zebrafish embryos caused by a combination of hypotonic stress and epithelial polarity defects.PLoS genetics · 2023Article
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- Tumor cell malignancy: A complex trait built through reciprocal interactions between tumors and tissue-body system.iScience · 2022Review
- Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022Review
- The polarity protein Par3 coordinates positively self-renewal and negatively invasiveness in glioblastoma.Cell death & disease · 2021Article
- Loss of polarity protein Par3, via transcription factor Snail, promotes bladder cancer metastasis.Cancer science · 2021Article
- Orchestration of tissue-scale mechanics and fate decisions by polarity signalling.The EMBO journal · 2021Review
- The polarity protein PARD3 and cancer.Oncogene · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma, an aggressive skin malignancy with increasing lifetime risk, originates from melanocytes (MCs) that are in close contact with surrounding epidermal keratinocytes (KCs). How the epidermal microenvironment controls melanomagenesis remains poorly understood. In this study, we identify an unexpected non-cell autonomous role of epidermal polarity proteins, molecular determinants of cytoarchitecture, in malignant melanoma. Epidermal Par3 inactivation in mice promotes MC dedifferentiation, motility, and hyperplasia and, in an autochthonous melanoma model, results in increased tumor formation and lung metastasis. KC-specific Par3 loss up-regulates surface P-cadherin that is essential to promote MC proliferation and phenotypic switch toward dedifferentiation. In agreement, low epidermal PAR3 and high P-cadherin expression correlate with human melanoma progression, whereas elevated P-cadherin levels are associated with reduced survival of melanoma patients, implying that this mechanism also drives human disease. Collectively, our data show that reduced KC Par3 function fosters a permissive P-cadherin-dependent niche for MC transformation, invasion, and metastasis. This reveals a previously unrecognized extrinsic tumor-suppressive mechanism, whereby epithelial polarity proteins dictate the cytoarchitecture and fate of other tissue-resident cells to suppress their malignant outgrowth.
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Registered trials
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.