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Published VersionCC BY-NC-ND V4.0, Open Access
Journal article
Host-defence caerin 1.1 and 1.9 peptides suppress B16 melanoma growth by inducing apoptosis and disrupting lipid metabolism
Biomedicine & Pharmacotherapy, Vol.189, pp.1-14
2025
PMID: 40516331
Abstract
Caerin peptides, originally isolated from the skin secretions of Australian tree frogs of the genus Litoria, have shown potential as anti-cancer agents in previous studies. This study investigates the impact of caerin 1.1 and 1.9 (F1/F3) peptides on lipid and amino acid metabolism in B16 melanoma cells, assessing their effects on cell proliferation and the tumour microenvironment (TME). F1/F3 significantly inhibited the proliferation of B16 cells in vitro, and metabolomic analysis revealed lipid metabolites, including lysophosphatidylcholines, phosphatidylcholines, phosphatidylethanolamines, and polyunsaturated fatty acids, were significantly downregulated in vivo in a murine model. Pathway enrichment analysis further highlighted suppressed fatty acid biosynthesis and unsaturated fatty acid synthesis, suggesting an impairment in lipid metabolic processes. Additionally, elevated levels of proinflammatory cytokine expression and inflammatory macrophage infiltration were observed in the TME, likely contributing to the enhanced anti-tumour response. Branched-chain amino acid degradation pathways were also less active in the F1/F3 group, suggesting altered acetyl-CoA availability impacting lipid synthesis. Notably, metabolites such as 3-Hydroxyvalproic acid and carnitine derivatives were markedly elevated, indicating potential antiproliferative and anti-inflammatory effects. These findings suggest that caerin peptides exert anti-cancer effects through multifaceted mechanisms, including modulation of lipid metabolism and immune activation, positioning caerin peptides as promising candidates for combination therapy in melanoma and potentially other malignancies.
Details
- Title
- Host-defence caerin 1.1 and 1.9 peptides suppress B16 melanoma growth by inducing apoptosis and disrupting lipid metabolism
- Authors
- Jiawei Fu - First Affiliated Hospital of Guangdong Pharmaceutical UniversityXinyi Song - First Affiliated Hospital of Guangdong Pharmaceutical UniversityRongmi Mo - The University of SydneyBernardo Cavallazzi Sebold - The University of SydneyYuandong Luo - Zhong′ao Biomedical Technology (Guangdong) Co. Ltd. (China)Junjie Li - Zhong′ao Biomedical Technology (Guangdong) Co. Ltd. (China)Quanlan Fu - Zhong′ao Biomedical Technology (Guangdong) Co. Ltd. (China)Hejie Li - University of the Sunshine Coast, Queensland, School of Science, Technology and EngineeringXiaosong Liu (Corresponding Author) - First Affiliated Hospital of Guangdong Pharmaceutical UniversityTianfang Wang (Corresponding Author) - University of the Sunshine Coast, Queensland, School of Science, Technology and EngineeringGuoying Ni (Corresponding Author) - First Affiliated Hospital of Guangdong Pharmaceutical University
- Publication details
- Biomedicine & Pharmacotherapy, Vol.189, pp.1-14
- Publisher
- Elsevier Masson
- Date published
- 2025
- DOI
- 10.1016/j.biopha.2025.118242
- ISSN
- 1950-6007; 0753-3322
- PMID
- 40516331
- Copyright note
- © 2025 Published by Elsevier Masson SAS. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-ncnd/4.0/).
- Data Availability
- I have shared my data at the Attach File step.
- Grant note
- This study was supported in part by National Natural Science Foundation of China (31971355), National Science Foundation of Guangdong province (2020A1515010855), and Deng Feng project of Foshan First People’s Hospital (2019A008).
- Organisation Unit
- School of Science and Engineering - Legacy; GeneCology Research Centre - Legacy; School of Science, Technology and Engineering; Centre for Bioinnovation
- Language
- English
- Record Identifier
- 991136299702621
- Output Type
- Journal article
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