ArticleInnovation (Cambridge (Mass.))2025
IFI30 promotes tumor-associated macrophage infiltration via activation of the ATF3-CCL5 axis in breast cancer.
Article in Innovation (Cambridge (Mass.)), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Immune Biomarkers of Islet Transplant Rejection Revealed by Synthetic Immunological Niche.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Immune Biomarkers of Islet Transplant Rejection Revealed by Synthetic Immunological Niche.bioRxiv : the preprint server for biology · 2026Article
- From State, Pathway, to Niche: The Ternary Network of Breast Cancer Stem-like Cells Driving Tumor Progression and Combination Therapy Prospects.Biomolecules · 2026Review
- Molecular Determinants of Macrophage Polarization in Glioblastoma and Implications for Tumor Progression.Cells · 2026Article
- Integrative analysis of scRNA-seq and bulk RNA-seq with machine learning develops a nucleotide metabolism-based prognostic model for ccRCC and reveals the function of IFI30.Frontiers in oncology · 2026Article
- NaResearch (Washington, D.C.) · 2025Article
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Authors and funding
12 authors.
Funding
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Abstract
Immunotherapy has transformed cancer treatment, but its effectiveness in breast cancer remains suboptimal. Tumor-associated macrophages (TAMs), a key component of the tumor microenvironment (TME), contribute significantly to immune evasion. In this study, we identified gamma-interferon-inducible lysosomal thiol reductase (IFI30) as a critical regulator of TAM function in breast cancer. IFI30 expression is upregulated in breast cancer via enhanced Histone 3 lysine 27 acetylation (H3K27ac) modification and promotes tumor progression and metastasis in an immune-dependent manner. Mechanistically, IFI30 in breast cancer cells recruits TAMs by activating the ATF3-CCL5 axis. Within macrophages, it promotes M2-like polarization and PD-L1 upregulation, fostering an immunosuppressive TME. Our findings established IFI30 as a promising therapeutic target for disrupting TAM-mediated immune suppression and enhancing breast cancer immunotherapy.
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