ArticleInternational journal of medical sciences2026
Melatonin inhibits FAK signaling to suppress PD-L1 expression and enhance chemosensitivity in triple-negative breast cancer.
Article in International journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Melatonin beyond chronobiology: integrating pharmacokinetics, dose-exposure forecasting, and clinical evidence.Molecular biology reports · 2026Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Triple-negative breast cancer (TNBC) is an aggressive subtype lacking targetable hormone receptors, making conventional chemotherapy the primary treatment option, despite its associated toxicity and potential for drug resistance. Melatonin, a natural hormone with anticancer and immunomodulatory properties, has shown promise in multiple cancers; however, its role in TNBC remains unclear. Methods: We analyzed serum melatonin levels in TNBC patients and healthy controls. The biological effects of melatonin were then evaluated in human (MDA-MB-231, MDA-MB-468) and murine (4T1) TNBC cell lines. Results: We found that TNBC patients had significantly lower serum melatonin levels than healthy controls. Conclusions: Melatonin suppresses TNBC progression by inhibiting proliferation and migration and by modulating the immune microenvironment through the FAK-PD-L1 axis. These findings highlight melatonin as a potential low-toxicity adjunct to enhance the efficacy of current TNBC therapies.
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