ArticleMediators of inflammation2016
Walker 256 Tumor Growth Suppression by Crotoxin Involves Formyl Peptide Receptors and Lipoxin A₄.
Article in Mediators of inflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Who cites it
10 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- Article
- Crotoxin induces cytotoxic effects in human malignant melanoma cells in both native and detoxified forms.Frontiers in pharmacology · 2024Article
- Article
- Antineoplastic properties and pharmacological applications of Crotalus durissus terrificus snake venom.Revista da Sociedade Brasileira de Medicina Tropical · 2022Review
- Crotoxin Modulates Events Involved in Epithelial-Mesenchymal Transition in 3D Spheroid Model.Toxins · 2021Article
- Crotoxin Inhibits Endothelial Cell Functions in Two- and Three-dimensional Tumor Microenvironment.Frontiers in pharmacology · 2021Article
- Crotoxin promotes macrophage reprogramming towards an antiangiogenic phenotype.Scientific reports · 2019Article
- Review
- The Walker 256 Breast Cancer Cell- Induced Bone Pain Model in Rats.Frontiers in pharmacology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the effects of Crotoxin (CTX), the main toxin of South American rattlesnake (Crotalus durissus terrificus) venom, on Walker 256 tumor growth, the pain symptoms associated (hyperalgesia and allodynia), and participation of endogenous lipoxin A4. Treatment with CTX (s.c.), daily, for 5 days reduced tumor growth at the 5th day after injection of Walker 256 carcinoma cells into the plantar surface of adult rat hind paw. This observation was associated with inhibition of new blood vessel formation and decrease in blood vessel diameter. The treatment with CTX raised plasma concentrations of lipoxin A4 and its natural analogue 15-epi-LXA4, an effect mediated by formyl peptide receptors (FPRs). In fact, the treatment with Boc-2, an inhibitor of FPRs, abolished the increase in plasma levels of these mediators triggered by CTX. The blockage of these receptors also abolished the inhibitory action of CTX on tumor growth and blood vessel formation and the decrease in blood vessel diameter. Together, the results herein presented demonstrate that CTX increases plasma concentrations of lipoxin A4 and 15-epi-LXA4, which might inhibit both tumor growth and formation of new vessels via FPRs.
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