ArticleBiomedicines2022
Human Lactoferrin Synergizes with Etoposide to Inhibit Lung Adenocarcinoma Cell Growth While Attenuating Etoposide-Mediated Cytotoxicity of Human Endothelial Cells.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- LFC-Lab on a chip · 2026Article
- Lactoferrin treatment activates acetylcholinesterase, decreasing acetylcholine levels in non-small cell lung cancer (NSCLC) cell culture supernatants, inhibiting cell survival.FEBS open bio · 2026Article
- Cytotoxic Effect of Escitalopram/Etoposide Combination on Etoposide-Resistant Lung Cancer.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Lactoferrin and Activated Protein C: Potential Role in Prevention of Cancer Progression and Recurrence.International journal of molecular and cellular medicine · 2023Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Lung cancer continues to be the deadliest cancer worldwide. A new strategy of combining chemotherapeutics with naturally occurring anticancer compounds, such as lactoferrin, might improve the efficacy and toxicity of current chemotherapy. The aim of this study was to evaluate the effect of recombinant human lactoferrin (rhLf) in combination with etoposide on anticancer activity in human lung adenocarcinoma cells. In addition, we examined the impact of rhLf on etoposide-induced cytotoxicity of human endothelial cells. We found that treatment of A549 cells with a combination of etoposide and rhLf resulted in significantly greater inhibition of cancer cell growth as compared to etoposide alone. The combination repressed cancer cell growth by cell cycle arrest in the G2/M phase and induction of apoptosis. In contrast to cancer cells, rhLf did not affect endothelial cell viability. Importantly, rhLf significantly diminished the etoposide-induced cytotoxicity of endothelial cells. Analysis of the type of drug interaction based on combination index value showed that rhLf synergized with etoposide to induce anticancer activity. The calculated dose reduction index indicated that the combination treatment reduced a 10-fold of etoposide dose to achieve the same anticancer effect. Our data demonstrate that rhLf enhanced the anticancer activity of etoposide and diminished etoposide-induced cytotoxic effect in endothelial cells.
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Registered trials
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