ArticleInternational journal of molecular sciences2025
Molecular Docking of Lactoferrin with Apoptosis-Related Proteins Insights into Its Anticancer Mechanism.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed.
- Role of arbutin and acetoside against Parkinson's disease.Indian journal of pharmacology · 2026Review
- Study of the potential protective efficacy of lactoferrin on indomethacin-induced gastric fundic mucosal injury in rats.Journal of molecular histology · 2026Article
- Liproxstatin-1 Protects SH-SY5Y Cells by Inhibiting HInternational journal of molecular sciences · 2025Article
- Special Issue "New Insights into Lactoferrin".International journal of molecular sciences · 2025Article
- Regulation of apoptosis and interaction with cartilage degeneration in osteoarthritis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human Lactoferrin (hLf), a multifunctional glycoprotein, has been analyzed through molecular docking to evaluate its role in apoptosis regulation and its potential as an anticancer agent. The docking results highlight XIAP (X-linked Inhibitor of Apoptosis Protein) and Caspase-3 as the most reliable targets, where hLf disrupts XIAP's inhibition of Caspase-3 and Caspase-9, potentially restoring apoptotic signaling; hLf also stabilizes Caspase-3, enhancing its activation in intrinsic and extrinsic pathways. Weaker interactions were observed with Fas, Bcl-2, and Akt. hLf's role in Fas signaling is likely due to expression upregulation rather than direct binding. In contrast, its binding to Bcl-2 may disrupt anti-apoptotic function, and its interaction with Akt suggests interference with pro-survival signaling. These findings suggest that hLf may promote apoptosis by enhancing caspase activation and modulating key apoptotic regulators, supporting its potential use in cancer treatment. However, further experimental validation is needed to confirm these interactions and their therapeutic implications.
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Registered trials
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