Introduction: Melittin, a 26-amino acid polypeptide with various pharmacological effects, possesses potential anti-tumor properties. The present study examined the possible mechanisms of action on Osteosarcoma (OS) cells. Materials and Methods: A series of in-vitro tests was implemented to investigate the effects of melittin on the survival, apoptosis, migration, and invasion of OS cells (143-B and MG63). An immunoblotting assay was applied to quantify the protein expression of potential mediators. Further, the mechanisms of action of melittin on OS cells were validated through rescue assays. Results: In OS cells 143-B and MG63, melittin treatment evidently reduced the cell viability, migration, and invasion and elevated apoptosis, with downregulated Bcl-2 and upregulated Bax and cleaved caspase-3. Moreover, the phosphorylation of PI3K/AKT/m- TOR was diminished following melittin treatment. In contrast, the rescue assay demonstrated that the anti-OS effects of melittin in vitro were negated by the 740 Y-P (a known PI3K activator). This was evidenced by altered viability, migration, and invasion, reduced apoptosis in OS cells, and the expression of apoptosis-related mediators. Discussion: Utilizing an in-vitro OS cell model, the current study discovered that melittin can suppress the growth, migration, and invasion of OS cells yet promote apoptosis, potentially via targeting PI3K/AKT/mTOR pathway, providing a novel mechanism underlying the effect of melittin on OS cells. Conclusion: The research demonstrated the anti-OS effects of melittin and its possible relationship with the PI3K/AKT/mTOR pathway.
Li et al. (Thu,) studied this question.