ArticleCell death & disease2026
The TRIM3/TLR3 axis overrides IFN-β feedback inhibition to suppress NSCLC progression.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
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Who cites it
2 citing papers in PubMed.
- Toll-like Receptor 3 as a Context-Dependent Molecular Switch in Epithelial Cancers: Balancing Cell Death and Tumor-Supportive Programs.International journal of molecular sciences · 2026Review
- TRIM family proteins: dual roles in tumor immunity.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Interferon-beta (IFN-β) has potent antitumor activity, but its clinical therapeutic potential is undermined by intrinsic negative feedback loops that suppress IFN-β production. However, the feedback mechanisms regulating IFN-β homeostasis in non-small cell lung cancer (NSCLC) remain unclear. We found that tripartite motif containing 3 (TRIM3) promotes the transcription and mRNA expression of IFNB1. Conversely, excessive IFN-β inhibits expression of TRIM3, creating their reciprocal feedback loop. Mass spectrometry revealed that toll-like receptor 3 (TLR3), a key sensor that triggers IFN-β production, is the interacting partner of TRIM3. Following the elucidation of the interactive mode between TRIM3 and TLR3, we found that activation of the TRIM3/TLR3 axis induced IFN-β secretion and overrode the feedback inhibition. Sustained IFN-β secretion subsequently inhibits NSCLC cell proliferation and reprograms the tumor microenvironment by increasing the infiltration levels of CD4
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