ArticleTranslational oncology2026
IL-32 drives PR3-dependent NET formation to promote portal vein tumor thrombosis and radioresistance in HCC.
Article in Translational oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIL-32 is a pro-inflammatory cytokine associated with chronic inflammation. Neutrophil extracellular traps (NETs) contribute to thrombosis, tumor invasion, and metastasis. This study investigated whether IL-32 derived from hepatocellular carcinoma (HCC) cells induces NET formation, promotes portal vein tumor thrombus (PVTT), and contributes to radiotherapy resistance.
methodsImmunofluorescence was used to assess co-localization of IL-32 and NET markers in tumor tissues. Mass cytometry analyzed immune cell composition in the tumor microenvironment. Neutrophils from healthy donors were used to evaluate NET formation. PAD4⁻/⁻ mice and DNase I treatment were used to assess NET function in vivo.
resultsIL-32 and NETs were significantly elevated and positively correlated in HCC, particularly in patients with PVTT. Tumor-derived IL-32 induced robust NET formation in a dose-dependent manner, which was markedly attenuated by PR3 inhibition, identifying PR3 as a critical mediator. In HCC and PVTT tissues, IL-32 co-localized with NET markers and was associated with increased neutrophil infiltration. In vivo, NET depletion significantly suppressed intrahepatic metastasis. Notably, radiotherapy further enhanced NET formation, and elevated IL-32-NET levels were associated with radioresistance in patients.
conclusionTumor-derived IL-32 drives PR3-dependent NET formation, promoting PVTT progression and contributing to radiotherapy resistance in HCC. Targeting the IL-32-PR3-NET axis may represent a potential therapeutic strategy.
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