ArticleNature communications2024
Cell state dependent effects of Bmal1 on melanoma immunity and tumorigenicity.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed, 20 citations in OpenAlex.
- Role of the circadian rhythm in squamous cell carcinoma: From molecular mechanism to therapy (Review).Molecular medicine reports · 2026Review
- Temporal dynamics in cancer immunotherapy: the interplay between circadian rhythms, tumor microenvironment, and immune checkpoint blockade.Journal of the National Cancer Center · 2026Review
- Molecular Mechanisms of Symptom Fluctuations in Malignant Tumor Patients: Stable by Day and Severe at Night.Journal of Cancer · 2026Review
- Circadian clock and cancer.Military Medical Research · 2026Review
- Life Factors and Melanoma: From the Macroscopic State to the Molecular Mechanism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Neuro-immune crosstalk in cancer: mechanisms and therapeutic implications.Signal transduction and targeted therapy · 2025Review
- Rapid and Inexpensive Image-Guided Grayscale Biomaterial Customization via LCD Printing.Journal of biomedical materials research. Part A · 2025Article
- Rhythm is essential: Unraveling the relation between the circadian clock and cancer.Critical reviews in oncology/hematology · 2025Review
- Basic helix-loop-helix ARNT like 1 regulates the function of immune cells and participates in the development of immune-related diseases.Burns & trauma · 2025Review
- Circadian system and aging: where both times interact.Frontiers in aging · 2025Review
- The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.Research (Washington, D.C.) · 2025Review
- Melatonin as an anti-inflammatory hormone bridging migraine relief and cancer immunity enhancement: a literature review.Frontiers in immunology · 2025Review
- Clocking Cancer Immunotherapy Responses.Cancer research · 2024Article
- Unveiling the enigmatic role of MYH9 in tumor biology: a comprehensive review.Cell communication and signaling : CCS · 2024Review
- Extracellular Vesicles, Circadian Rhythms, and Cancer: A Comprehensive Review with Emphasis on Hepatocellular Carcinoma.Cancers · 2024Review
- Crosstalk between Circadian Rhythm Dysregulation and Tumorigenesis, Tumor Metabolism and Tumor Immune Response.Aging and disease · 2024Review
- Biological clock regulation by theFrontiers in cell and developmental biology · 2024Review
- FA-PEG Modified ZIF(Mn) Nanoparticles Loaded with Baicalin for Imaging-Guided Treatment of Melanoma in Mice.International journal of nanomedicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 6 institutions in 1 country.
Funding
Abstract
The circadian clock regulator Bmal1 modulates tumorigenesis, but its reported effects are inconsistent. Here, we show that Bmal1 has a context-dependent role in mouse melanoma tumor growth. Loss of Bmal1 in YUMM2.1 or B16-F10 melanoma cells eliminates clock function and diminishes hypoxic gene expression and tumorigenesis, which could be rescued by ectopic expression of HIF1α in YUMM2.1 cells. By contrast, over-expressed wild-type or a transcriptionally inactive mutant Bmal1 non-canonically sequester myosin heavy chain 9 (Myh9) to increase MRTF-SRF activity and AP-1 transcriptional signature, and shift YUMM2.1 cells from a Sox10
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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.