ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026
Tumor-Derived Alpha-1 Antitrypsin Promotes Liver Metastasis of Colorectal Cancer Through the Neutrophil Extracellular Traps-CCDC25 Pathway.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Tumor-Derived Alpha-1 Antitrypsin Promotes Liver Metastasis of Colorectal Cancer Through the Neutrophil Extracellular Traps-CCDC25 Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Liver metastasis is a leading cause of mortality in colorectal cancer (CRC), where the inflammatory tumor microenvironment, specifically neutrophil infiltration, significantly promotes metastatic colonization. This study reveals a pro-metastatic role for alpha-1 antitrypsin (A1AT) in CRC liver metastasis via a dual mechanism involving neutrophil extracellular traps (NETs) and the transmembrane protein coiled-coil domain-containing protein 25 (CCDC25). We demonstrate that A1AT, highly expressed by a liver-metastatic CRC cell line established in a mouse model, directly induces NETs' formation. Simultaneously, intracellular A1AT binds to CCDC25, preventing its lysosomal degradation and thereby increasing its surface expression. This A1AT-mediated upregulation of CCDC25 sensitizes tumor cells to surrounding NET-DNA. Upon engagement, the ILK-RAC1-CDC42 signaling cascade activates, driving extensive cytoskeletal rearrangement and enhancing the migratory and invasive capabilities of CRC cells. Collectively, our findings elucidate a mechanism wherein tumor cells exploit the A1AT-NET-CCDC25 axis to manipulate neutrophil function and boost metastatic potential. This axis represents a critical driver of CRC liver metastasis, offering novel biomarkers and promising therapeutic targets.
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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 Socratic graph.