ArticleBiology direct2025
CLOCK-mediated acetylation of NF-κB p65 drives immune evasion in breast cancer.
Article in Biology direct, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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
6 citing papers in PubMed.
- Functional deficiency of circadian regulator PER2 enhances breast cancer susceptibility and progression with immunosuppression.Oncogene · 2026Article
- Osteopontin Promotes Lung Cancer Growth through NF-κB-Dependent Upregulation of PD-L1 and Suppression of Anti-Tumor Immunity.Molecular biology reports · 2026Article
- Postbiotics Against Breast Cancer: A Narrative Review Bridging Preclinical Evidence with Potential Clinical Application.Cancers · 2026Review
- Can Disruption of Circadian Rhythms Be Linked to Radiation-Induced Acute Myeloid Leukaemia?Cancers · 2026Review
- Circadian Rhythms in Colorectal Cancer: Recent Advances in Development and Treatment.Journal of clinical medicine research · 2026Review
- Synchronizing immunity with time: unlocking the potential of chrono-immunotherapy in cancer.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDisruption of circadian rhythm (DCR) has been connected with breast cancer (BC) susceptibility; whereas it is unclear whether status of key clock genes could be used in predicting BC prognosis, tumor immune microenvironment, and immunotherapy responses.
resultsCircadian clock genes demonstrate significant dysregulation in BC, where elevated CLOCK expression emerges as an independent prognostic factor strongly correlated with adverse clinical outcomes. CLOCK-overexpressing BC cells exhibit enhanced proliferative ability and strong resistance to chemotherapy drugs doxorubicin and gemcitabine. High CLOCK expression correlates with reduced CD8
conclusionsCLOCK functions as a critical prognostic biomarker in BC by promoting tumor proliferation, chemoresistance, and immune evasion. Mechanistically, CLOCK mediates NF-κB p65 acetylation to enhance PD-L1 transcription, promoting immune evasion in BC.
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Registered trials
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