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An In Vitro Laboratory Exploration Revealed the Antitumor Effects of Melittin on Osteosarcoma Cells
Yumei Li1, Xiaoliang Xie1, Haixia Zhu1
1Department of Orthopedics, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, China.
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:
In the beginning, the proliferation of human osteoblast precursor cell line hFOB 1.19 was assessed. 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 level of PI3K/AKT/ mTOR 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.
Insights
Melittin effectively inhibits Osteosarcoma (OS) cell growth, migration, and invasion while promoting apoptosis. This action is linked to the downregulation of the PI3K/AKT/mTOR pathway, offering a new therapeutic strategy for OS.
Area of Science:
- Biochemistry
- Molecular Biology
- Oncology
Background:
- Melittin, a polypeptide from bee venom, exhibits diverse pharmacological activities.
- Potential anti-tumor properties of melittin warrant investigation against various cancers.
- Osteosarcoma (OS) remains a significant challenge in orthopedic oncology.
Purpose of the Study:
- To elucidate the anti-cancer mechanisms of melittin in Osteosarcoma (OS) cells.
- To investigate the role of the PI3K/AKT/mTOR pathway in melittin's anti-OS effects.
- To evaluate melittin's impact on OS cell viability, apoptosis, migration, and invasion.
Main Methods:
- In-vitro assays were used to assess melittin's effects on OS cell lines (143-B and MG63).
- Immunoblotting quantified key protein expression, including apoptosis markers and pathway mediators.
- Rescue assays with a PI3K activator (740 Y-P) validated the role of the PI3K/AKT/mTOR pathway.
Main Results:
- Melittin significantly reduced OS cell viability, migration, and invasion.
- Melittin treatment increased apoptosis, evidenced by altered Bcl-2, Bax, and cleaved caspase-3 expression.
- Melittin suppressed PI3K/AKT/mTOR pathway phosphorylation, an effect reversed by 740 Y-P.
Conclusions:
- Melittin demonstrates potent anti-Osteosarcoma activity in vitro.
- The anti-cancer effects of melittin are mediated through the inhibition of the PI3K/AKT/mTOR signaling pathway.
- Melittin represents a potential therapeutic agent for Osteosarcoma, targeting key cell survival pathways.
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