ArticleBritish journal of cancer2025
TRIM26 deficiency potentially suppresses colorectal cancer liver metastasis through NF-κB-mediated M1-like tumor-associated macrophage polarization.
Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- TRIM26 triggers ferroptosis via ZEB1 degradation to suppress nasopharyngeal carcinoma progression.Journal of molecular histology · 2026Article
- TRIM26 deficiency promotes liver fibrosis progression by mediating macrophage polarization via the EZH2-STAT1 axis.Hepatology international · 2026Article
- Aberrant expression of TRIM26 suppresses ferroptosis through regulating GPX4 protein stability in colorectal cancer.Molecular biology reports · 2026Article
- E2F3 activates NF-κB signaling through TRIM26 mediated TAB1 ubiquitination in pancreatic cancer.International journal of biological sciences · 2026Article
- Transcriptomic Analysis Reveals the Role ofHuman mutation · 2026Article
- TRIM47: molecular characteristics, disease-related mechanisms, and clinical translational value.Frontiers in immunology · 2026Review
- Navigating the Tumor Microenvironment in Colorectal Liver Metastasis: Barriers to Therapy and Emerging Opportunities.Oncology research · 2026Review
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Authors and funding
11 authors.
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Abstract
backgroundColorectal cancer liver metastasis (CRLM) remains a major challenge in oncology, with the tumor microenvironment playing a crucial role in disease progression. This study investigates the function of the Tripartite Motif Containing 26 (TRIM26) in the CRLM microenvironment, focusing on its regulation of tumor-associated macrophage (TAM) polarization and its implications for metastatic growth.
methodsUsing established mouse CRLM models, we characterized TAM phenotypes using flow cytometry and immunohistochemistry. In vitro co-culture experiments evaluated the effects of Trim26-deficient bone marrow-derived macrophages (BMDMs) on tumor cell behavior. Western blotting and luciferase reporter assays were employed to elucidate the underlying molecular mechanisms.
resultsTrim26 knockout mice exhibited significantly reduced liver metastasis and an increased proportion of M1-like TAMs. Trim26-deficient BMDMs suppressed tumor cell migration and proliferation. TRIM26 modulates macrophage polarization by inhibiting the NF-κB signaling pathway. Specifically, TRIM26 interacts with TRAF2 through its PRY domain and inhibits the K63-linked ubiquitination of TRAF2, thereby attenuating NF-κB pathway activation. Furthermore, clinical CRLM samples revealed a negative correlation between TRIM26 expression and M1-like TAM infiltration.
conclusionWe identified TRIM26 as a potential therapeutic target for CRLM, providing novel insights into tumor-stromal microenvironment interactions and offering new strategies to improve patient outcomes.
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