ArticleiScience2026
CFIm25-dependent alternative polyadenylation in AKT2 mRNA programs macrophage polarization.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
- The distinguished predictive value of CFIm25 in schistosomal and non-schistosomal colorectal cancer.Translational cancer research · 2026Article
- The alternative polyadenylation factor CFIm25 orchestrates macrophage antibacterial activity againstInfection and immunity · 2026Article
- MiR-143-5p serves as a diagnostic biomarker in patients with sepsis and regulates sepsis-induced inflammation and cardiac dysfunction.Hereditas · 2025Article
Corrections and comments
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4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage polarization into M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes is essential for immune responses and tissue homeostasis. While transcriptional and post-transcriptional mechanisms controlling this process have been characterized, the contribution of alternative mRNA polyadenylation (APA) to polarization requires clarification. Using human monocytic cell lines, we demonstrate that CFIm25, a key APA regulator, controls macrophage polarization states. CFIm25 overexpression enhances M1 characteristics, including nitric oxide production, CD80 expression, pro-inflammatory cytokine secretion, phagocytosis, migration, and cancer cell killing, while suppressing M2 traits. CFIm25 knockdown produces opposite effects. Mechanistically, CFIm25 promotes the proximal polyadenylation of AKT2 mRNA, generating shorter transcripts with enhanced stability and translational efficiency that increase Akt2 protein levels and amplify NF-κB signaling. Blocking the proximal site with antisense oligonucleotides reduces Akt2 expression and induces M2-like phenotypes. These findings establish APA as a critical regulator of macrophage polarization and identify the CFIm25-Akt2-NF-κB axis as a potential therapeutic target for modulating immune responses.
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Registered trials
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