ArticleRedox report : communications in free radical research2023
Melittin kills A549 cells by targeting mitochondria and blocking mitophagy flux.
Article in Redox report : communications in free radical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Atractylodes macrocephala polysaccharide orchestrates anti-tumor immunity via a dual-network mechanism targeting the gut microbiota and spleen.NPJ biofilms and microbiomes · 2026Article
- Targeting oral squamous cell carcinoma with venom peptides: mechanisms, selectivity and translational potential.The protein journal · 2026Review
- Antimelanoma Activity of the Mastoparan Peptides MPX and MP1: Cellular Selectivity and Mechanism of Action.Molecular pharmaceutics · 2026Article
- Concentration-Dependent Anticancer Effects of Melittin-Functionalized Nanomaterials.Materials (Basel, Switzerland) · 2026Review
- Melittin Acts as a Radiosensitizer for Non-Small Cell Lung Cancer by Inhibiting the DNA Damage Repair System and Inducing Apoptosis.Yonsei medical journal · 2026Article
- Nanocarrier-Enabled Melittin Therapy: Mechanistic Advances, Therapeutic Applications, and Translational Challenges.International journal of nanomedicine · 2026Review
- Melittin inhibits NSCLC metastasis by targeting USP10 and promoting RNF20-mediated ubiquitination and degradation of PSMA7.Journal of translational medicine · 2025Article
- Pro-Apoptotic and Cytotoxic Effects of Melittin on HL-60 Acute Promyelocytic Leukemia Cells: Implications for Retinoid-Independent Therapy.Molecules (Basel, Switzerland) · 2025Article
- Therapeutic Bioactivity Exerted by theMolecules (Basel, Switzerland) · 2025Article
- Molecular regulation of mitophagy signaling in tumor microenvironment and its targeting for cancer therapy.Cytokine & growth factor reviews · 2025Review
- Development of a prognostic model based on seven mitochondrial autophagy- and ferroptosis-related genes in lung adenocarcinoma.BMC medical genomics · 2025Article
- Melittin-Based Nanoparticles for Cancer Therapy: Mechanisms, Applications, and Future Perspectives.Pharmaceutics · 2025Review
- Synthesis and characterization of honey bee venom-loaded calcium oxide nanocomposites and evaluation of their cytotoxic (MCF-7) and antifungal activity.Discover nano · 2025Article
- Antioxidant Peptides from the Fruit Source of the Oil CropFoods (Basel, Switzerland) · 2025Article
- The Role of Flexibility in the Bioactivity of Short α-Helical Antimicrobial Peptides.Antibiotics (Basel, Switzerland) · 2025Review
- Granzyme B and melittin in cancer immunotherapy: molecular mechanisms and therapeutic perspectives in head and neck cancers.Frontiers in immunology · 2025Review
- Melittin Inhibits Colorectal Cancer Growth and Metastasis by Ac-Tivating the Mitochondrial Apoptotic Pathway and Suppressing Epithelial-Mesenchymal Transition and Angiogenesis.International journal of molecular sciences · 2024Article
- Advances of E3 ligases in lung cancer.Biochemistry and biophysics reports · 2024Review
- Bee Venom: Composition and Anticancer Properties.Toxins · 2024Review
- Insights into the role of mitophagy in lung cancer: current evidence and perspectives.Frontiers in pharmacology · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melittin, a naturally occurring polypeptide found in bee venom, has been recognized for its potential anti-tumor effects, particularly in the context of lung cancer. Our previous study focused on its impact on human lung adenocarcinoma cells A549, revealing that melittin induces intracellular reactive oxygen species (ROS) burst and oxidative damage, resulting in cell death. Considering the significant role of mitochondria in maintaining intracellular redox levels and ROS, we further examined the involvement of mitochondrial damage in melittin-induced apoptosis in lung cancer cells. Our findings demonstrated that melittin caused changes in mitochondrial membrane potential (MMP), triggered mitochondrial ROS burst (Figure 1), and activated the mitochondria-related apoptosis pathway Bax/Bcl-2 by directly targeting mitochondria in A549 cells (Figure 2). Further, we infected A549 cells using a lentivirus that can express melittin-Myc and confirmed that melittin can directly target binding to mitochondria, causing the biological effects described above (Figure 2). Notably, melittin induced mitochondrial damage while inhibiting autophagy, resulting in abnormal degradation of damaged mitochondria (Figure 5). To summarize, our study unveils that melittin targets mitochondria, causing mitochondrial damage, and inhibits the autophagy-lysosomal degradation pathway. This process triggers mitoROS burst and ultimately activates the mitochondria-associated Bax/Bcl-2 apoptotic signaling pathways in A549 cells.
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