Publication: Melittin from apis florea venom as a promising anticancer agent
Issued Date
2020-08-01
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20796382
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2-s2.0-85089654342
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Mahidol University
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SCOPUS
Bibliographic Citation
Antibiotics. Vol.9, No.8 (2020), 1-18
Suggested Citation
Sirikwan Sangboonruang, Kuntida Kitidee, Panuwan Chantawannakul, Khajornsak Tragoolpua, Yingmanee Tragoolpua Melittin from apis florea venom as a promising anticancer agent. Antibiotics. Vol.9, No.8 (2020), 1-18. doi:10.3390/antibiotics9080517 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/58973
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Title
Melittin from apis florea venom as a promising anticancer agent
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Abstract
© 2020 by the authors. Licensee MDPI, Basel, Switzerland. Melittin, a major component found in bee venom, is produced by the Apis species of the honey bee. In this study, the effect of melittin derived from Apis florea (Mel-AF), which is a wild honey bee species that is indigenous to Thailand, was investigated against human malignant melanoma (A375) cells. In this study, Mel-AF exhibited considerable potential in the anti-proliferative action of A375 cells. Subsequently, the cellular mechanism of Mel-AF that induced cell death was investigated in terms of apoptosis. As a result, gene and protein expression levels, which indicated the activation of cytochrome-c release and caspase-9 expression, eventually triggered the release of the caspase-3 executioner upon Mel-AF. We then determined that apoptosis-mediated cell death was carried out through the intrinsic mitochondrial pathway. Moreover, advanced abilities, including cell motility and invasion, were significantly suppressed. Mel-AF manipulated the actin arrangement via the trapping of stress fibers that were found underneath the membrane, which resulted in the defective actin cytoskeleton organization. Consequently, the expression of EGFR, a binding protein to F-actin, was also found to be suppressed. This outcome strongly supports the effects of Mel-AF in the inhibition of progressive malignant activity through the disruption of actin cytoskeleton-EGFR interaction and the EGFR signaling system. Thus, the findings of our current study indicate the potential usefulness of Mel-AF in cancer treatments as an apoptosis inducer and a potential actin-targeting agent.