ArticleScience China. Life sciences2026
EID1 blockade potentiates immunosurveillance against cancer metastasis via FPR1-mediated DC-NK crosstalk.
Article in Science China. Life 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.
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Who cites it
1 citing paper in PubMed.
- Disinhibiting dendritic cell-natural killer cell cooperation against metastasis.Immunity & inflammation · 2026Article
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Authors and funding
17 authors.
Funding
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Abstract
Metastatic disease remains the primary cause of cancer mortality, yet the identification of robust therapeutic targets is hampered by tumor heterogeneity and microenvironmental complexity. A key challenge lies in identifying epigenetic regulators that can simultaneously inhibit tumor progression and harness immunity. Here, we leverage single-cell transcriptomics from 120 liver cancer patients to identify E1A-like inhibitor of differentiation 1 (EID1) as the sole histone acetylation regulator upregulated in both tumor cells and effector lymphocytes within metastatic sites. Systemic Eid1 deletion markedly suppresses lung metastasis in melanoma, liver cancer, and breast cancer models. This protection is mediated dominantly by natural killer (NK) cells and type I/II interferons (IFNs), as evidenced by antibody-based cell depletion and cytokine neutralization. Eid1-deficient NK cells exhibit a hyperactivated state with robust proliferation, and their adoptive transfer confers superior metastatic suppression. Notably, Eid1 deficiency augments the accumulation of NK cells and dendritic cells (DCs) in lung metastases and induces a close spatial and transcriptional DC-NK interplay for metastatic defense. Mechanistically, loss of Eid1 upregulates formyl peptide receptor 1 (FPR1) and its ligand annexin A1 (ANXA1) on DCs and NK cells, enabling a FPR1-dependent DC-NK crosstalk that strengthens type I and II IFN responses against tumor dissemination. Conditional knockout demonstrated that intratumoral accumulation of NK cells and DCs is determined by cell-intrinsic Eid1. Critically, targeted Eid1 silencing delivered by nanoparticles significantly enhanced Fpr1 expression and NK activation, eventually suppressing tumor dissemination. Collectively, our study uncovers a previously unrecognized role of EID1 in promoting cancer metastasis by dampening the DC-NK joint immunosurveillance and establishes the therapeutic potential of EID1 inhibition in NK cell transfer and siRNA-based strategies.
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Registered trials
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