ArticleDiscover oncology2025
CXCL10/CXCR3 axis facilitates the M2 polarization of macrophages in colorectal cancer via activating RAF.
Article in Discover oncology, 2025. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Article
- Cytokines and Chemokines as Emerging Biomarkers and Therapeutic Targets in Colorectal Cancer-Narrative Review.International journal of molecular sciences · 2026Review
- High-Throughput Heterospheroid-Based Screening Identifies Drugs That Reprogram Tumor-Associated Macrophages.Journal of immunology research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Colorectal cancer (CRC) is a common malignant tumor with high incidence and mortality. Tumor-associated macrophages (TAMs) play a crucial role in CRC progression, with M2 polarization promoting CRC development. The present study explored the role of the CXCL10/CXCR3 axis in the M2 polarization of TAMs in CRC. Bioinformatics analysis of three gene expression omnibus (GEO) datasets identified differentially expressed genes, with CXCL10 selected as a target due to its upregulation in CRC and various cancers via the Cancer Genome Atlas (TCGA) database mining. Subsequent experiments demonstrated that CRC cells overexpressed CXCL10, which promoted M2 polarization of macrophages by activating the rapidly accelerated fibrosarcoma (RAF)/extracellular signal-regulated kinase (ERK) pathway. CXCL10-overexpressed CRC cells increased M2 macrophage markers like CD206 and arginase 1 (Arg1), reduced M1 markers CD86 and inducible nitric oxide synthase (iNOS), and enhanced interleukin-10 (IL-10) release while decreasing IL-6 and tumor necrosis factor-alpha (TNF-α). CXCL10-overexpressed CRC cells also inhibited macrophage phagocytic capacity and lysosomal enzyme activity, crucial for tumor immunotherapy. Furthermore, macrophages stimulated by CXCL10-overexpressed CRC cells facilitated CRC cell proliferation and invasion. Inhibitors of CXCR3 or RAF reversed these effects, confirming that CXCL10 promoted M2 polarization via the CXCR3/RAF/ERK pathway. Overall, the CXCL10/CXCR3 axis played a key role in CRC progression by inducing M2 polarization of macrophages via the RAF/ERK pathway, suggesting that CXCL10/CXCR3 axis may be a potential therapeutic target for CRC immunotherapy.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.