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Abstract

Cancer remains a threat to human life, affecting millions of people. Limitations associated with conventional tumor therapies motivate the search for new, effective, and non-toxic therapies. Cathelicidin peptide (CATH) is a host defense peptide with anti-microbial and immunomodulatory activity. Moreover, cumulative studies have revealed its anti-cancer properties. While several studies have explored their antimicrobial and anti-tumor potential, further research is needed to elucidate their specific mechanisms across different tumor types. Our study aimed to investigate the anti-cancer effects of two types of Chicken CATH, 1 and 2, on breast MCF-7, colon HCT-116, and liver HEPG-2 carcinoma cells, and to examine their impact on innate and adaptive immunity parameters. Using the WST-1 assay, treatment with chicken CATHs demonstrated a dose-dependent cytotoxic effect against MCF-7, HCT-116, and HEPG-2 cells. A dose of 20 μg /ml for both CATH peptides was determined for further experiments. The cell cycle distribution assay revealed that CATH had an anti-proliferative effect, resulting in cell cycle arrest at the G1/S phase in all three cancer cell lines. Using the Annexin V assay, treatment with either CATH-1 or CATH-2 significantly enhanced apoptotic cell death in all cancer cells. Finally, our data revealed no significant effect of either CATH peptide on activating human peripheral blood mononuclear cells (PBMNCs), as assessed by their impact on TNF and IFN-γ levels using flow cytometry. Additionally, CATHs had no effect on the gene expression levels of lymphocytic granzymes. In conclusion, we demonstrate that chicken CATH exhibits anti-tumor effects on cancer cells by targeting cancer hallmarks, including those beyond immunomodulation. Further studies, in combination with other therapies, can elucidate the potential of these peptides in cancer therapeutics

First Page

183

Last Page

192

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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