ReviewFrontiers in endocrinology2026
The circadian-melatonin axis in breast cancer metastasis: molecular mechanisms, organ-specific metastatic niches, and therapeutic opportunities.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer metastasis remains the leading cause of disease-related mortality despite major advances in systemic therapy. Increasing evidence indicates that the circadian-melatonin axis may influence metastatic progression by coordinating endocrine signaling, metabolism, immune responses, and tumor cell plasticity. In this review, we summarize current epidemiological, mechanistic, and translational evidence linking circadian disruption and melatonin to breast cancer metastasis. We discuss how core circadian clock genes and melatonin signaling may influence epithelial-mesenchymal transition, cancer stemness, circulating tumor cell dissemination, tumor metabolism, and immune remodeling. We further highlight the emerging potential roles of melatonin in shaping adipocyte-tumor crosstalk and organ-specific metastatic niches, including bone, lung, liver, and brain, where tissue-specific interactions may influence metastatic colonization. Finally, we discuss the clinical potential of circadian chronotherapy, adjuvant melatonin, and circadian biomarker-guided precision medicine. Although substantial experimental evidence supports the anti-metastatic properties of the circadian-melatonin axis, clinical translation remains limited by context-dependent biological effects and the lack of chronobiology-informed trials. Future studies integrating circadian biomarkers with optimized treatment timing and modern systemic therapies may facilitate precision strategies for preventing and treating metastatic breast cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.