ArticleOncoimmunology2016
Phorbol ester-induced neutrophilic inflammatory responses selectively promote metastatic spread of melanoma in a TLR4-dependent manner.
Article in Oncoimmunology, 2016. 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, 17 citations in OpenAlex.
- Uncovering the Intricate and Heterogeneous Cellular Microenvironment of Cutaneous Melanoma.Medicina (Kaunas, Lithuania) · 2026Review
- Neutrophils activated by membrane attack complexes increase the permeability of melanoma blood vessels.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Tat-thioredoxin 1 reduces inflammation by inhibiting pro-inflammatory cytokines and modulating MAPK signaling.Experimental and therapeutic medicine · 2021Article
- Oleic acid-containing semisolid dosage forms exhibit in vivo anti-inflammatory effect via glucocorticoid receptor in a UVB radiation-induced skin inflammation model.Inflammopharmacology · 2020Article
- TLR4 in skin cancer: From molecular mechanisms to clinical interventions.Molecular carcinogenesis · 2019Article
- NO-dependent attenuation of TPA-induced immunoinflammatory skin changes in Balb/c mice by pindolol, heptaminol or ATRA, but not by verapamil.Oncotarget · 2016Article
- Tea polyphenols inhibit the proliferation, migration, and invasion of melanoma cells through the down-regulation of TLR4.International journal of immunopathology and pharmacologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increased neutrophil counts both in tumor tissue and peripheral blood correlate with poor clinical outcome in melanoma patients suggesting a pro-tumorigenic role of neutrophils for the pathogenesis of malignant melanoma. Recently, we discovered that neutrophilic skin inflammatory responses induced by UV exposure promote metastatic spread of primary cutaneous melanomas in genetically engineered Hgf-Cdk4(R24C) mice. We hypothesized that other pro-inflammatory stimuli that induce neutrophilic inflammatory responses also promote the development and progression of melanomas. In the current study, we therefore investigated how the most potent and frequently used tumor promoter 12-O-Tetradecanoylphorbol-13-acetate (TPA) affects the development and progression of carcinogen-induced melanomas in Hgf-Cdk4(R24C) mice. Local and systemic neutrophilic inflammatory responses induced by TPA also selectively increase the metastatic spread of melanoma cells to draining lymph nodes and lungs. Using a highly metastatic Hgf-Cdk4(R24C) melanoma skin transplant we could show that TPA enhances systemic spread of melanoma cells which was depended on intact TLR4 signaling in recipient mice and on the presence of neutrophils. Altogether, our experimental results support an important mechanistic role of TLR4-driven neutrophilic inflammation for melanoma progression.
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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.