ArticleYonsei medical journal2026
Melittin Acts as a Radiosensitizer for Non-Small Cell Lung Cancer by Inhibiting the DNA Damage Repair System and Inducing Apoptosis.
Article in Yonsei medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Mechanisms of In Vitro Cytotoxicity of Honeybee Venom Components and Melittin-Functionalized FeMaterials (Basel, Switzerland) · 2026Article
- From Toxin to Therapy: Biomedical Applications of Bee Venom in Cancer, Diabetes, and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Pharmacological Properties and Phytochemical Profile ofMarine drugs · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
purposeThis study aimed to evaluate the radiosensitizing effects of melittin, the main active component of bee venom, in non-small cell lung cancer (NSCLC) cells. Given the limitations of radiotherapy due to intrinsic tumor resistance, we investigated whether melittin could enhance the efficacy of radiation by promoting apoptosis and impairing DNA damage repair mechanisms. MATERIALS AND
methodsNSCLC cell lines were treated with melittin and exposed to ionizing radiation. Clonogenic assays assessed radiosensitivity, while Western blot analyses examined DNA damage response proteins (DNA-PKcs, ATM, γ-H2AX) and apoptosis markers (Bax, cleaved caspase-3). In vivo, a BALB/c nude mouse xenograft model was used to evaluate the therapeutic effect of combined treatment. Tumor volume, weight, and immunohistochemical (IHC) staining were analyzed.
resultsMelittin significantly enhanced radiosensitivity in NSCLC cells, as indicated by decreased colony formation. It reduced phosphorylation of DNA-PKcs and ATM while increasing γ-H2AX, suggesting impaired DNA double-strand break repair. Apoptotic activity increased with elevated Bax and cleaved caspase-3 levels. In vivo, combination therapy markedly inhibited tumor growth, as supported by IHC evidence of increased apoptosis and DNA damage.
conclusionMelittin is a potent radiosensitizer in NSCLC, impairing DNA repair and promoting apoptosis. These findings support its potential as a novel adjunct to radiotherapy to improve NSCLC treatment outcomes.
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