Abstract
The cytotoxic effects of melittin, a bee-venom peptide, have been widely studied towards cancer cells. Typically, these studies have examined the effect of melittin over extended-time courses (6–24 hours), meaning that immediate cellular interactions have been overlooked. In this work, we demonstrate the rapid effects of melittin on both gastric and colorectal cancer, specifically AGS, COLO205 and HCT-15 cell lines, over a period of 15 minutes. Melittin exhibited a dose dependent effect at 4 hours of treatment, with complete cellular death occurring at the highest dose of 20 μg/mL. Interestingly, when observed at shorter time points, melittin induced cellular changes within seconds; membrane damage was observed as swelling, breakage or blebbing. High-resolution imaging revealed treated cells to be compromised, showing clear change in cellular morphology. After 1 minute of melittin treatment, membrane changes were observed, and intracellular material could be seen expelled from the cells. Overall, these results enhance our understanding of the fast acting anti-cancer effects of melittin.
Highlights
Cancer is a leading cause of mortality worldwide, currently accounting for approximately 1 in 6 deaths [1]
To identify the concentration range at which melittin causes cancer cell death, cytotoxicity was measured through propidium iodide (PI) uptake by non-viable cells and analysed by FACS
Assessment of cellular viability as a function of melittin concentration revealed that the effective concentration range for all cancer types was between 5–20 μg/mL, with 24.8 ± 9.4%, 31.2 ± 17% and 43.9 ± 12.4% cell death seen for at shorter treatment times. Gastric (AGS), HCT-15 and COLO205 respectively for the 10μg/mL treatment (P = 0.0009)
Summary
Cancer is a leading cause of mortality worldwide, currently accounting for approximately 1 in 6 deaths [1]. A recent report by the World Health Organisation (WHO) estimated that in 2018 18 million cases of cancer were diagnosed, and 9.6 million cancer related deaths occurred. Colorectal and gastric cancers are the third and fifth most commonly diagnosed cancers, accounting for 10% and 6% of cancer diagnoses, respectively. It is unsurprising that these cancer types are responsible for high mortality rates, largely due to their poor prognosis [1]. Cancer therapies consist mainly of surgical intervention, chemo- or radio-therapy, and gene or hormone therapy. There is still a distinct lack of targeted treatments available despite recent developments, including antibody therapeutics, peptides and other small molecule therapeutics [2,3,4]
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