Cytotoxic effects of Chartergellus communis wasp venom peptide against melanoma cells
Cancer is a huge public health problem being one of the main causes of death globally. Specifically, melanoma is one of the most threatening cancer types due to the metastatic capacity, treatment resistance and mortality rates. It is evident the urgent need for research on new agents with pharmacolo...
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Veröffentlicht in: | Biochimie 2024-01, Vol.216, p.99-107 |
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Sprache: | eng |
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Zusammenfassung: | Cancer is a huge public health problem being one of the main causes of death globally. Specifically, melanoma is one of the most threatening cancer types due to the metastatic capacity, treatment resistance and mortality rates. It is evident the urgent need for research on new agents with pharmacological potential for cancer treatment, in order to develop new cancer therapeutic strategies and overcome drug resistance. The present work investigated the anti-tumoral potential of Chartergellus-CP1 peptide, isolated from Chartergellus communis wasp venom on human melanoma cell lines with different pigmentation degrees, namely the amelanotic cell line A375 and pigmented cell line MNT-1. Chartergellus-CP1 induced selective cytotoxicity to melanoma cell lines when compared to the lower induced cytotoxicity towards to nontumorigenic keratinocytes. Chartergellus-CP1 peptide induced apoptosis in both melanoma cell lines, cell cycle impairment in amelanotic A375 cells and intracellular ROS increase in pigmented MNT-1 cells. The amelanotic A375 cell line showed higher sensitivity to the peptide than the pigmented cell line MNT-1. From our knowledge, this is the first study reporting the cytotoxicity effects of Chartergellus-CP1 on melanoma cells.
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•Chartergellus-CP1 peptide induced selective anti-tumoral toxicity on melanoma cells.•Cytotoxic mechanisms are mainly related to oxidative stress and apoptotic death.•Chartergellus-CP1 may represent a novel therapeutic strategy on melanoma treatment. |
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ISSN: | 0300-9084 1638-6183 |
DOI: | 10.1016/j.biochi.2023.10.015 |