ArticleMolecular cancer2025
ADAR1-high tumor-associated macrophages induce drug resistance and are therapeutic targets in colorectal cancer.
Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Berberine suppresses colorectal cancer progression by inducing ferroptosis-mediated energy metabolism disorders.Journal of advanced research · 2026Article
- Multidrug resistance in cancer: current understandings and future perspective.Molecular biomedicine · 2026Review
- Extracellular vesicles in solid tumors: from tumor ecology to engineered therapeutics.Molecular cancer · 2026Review
- Targeting ADAR1 lactylation activates innate immune and overcomes chemoresistance in ovarian cancer.Cell death and differentiation · 2026Article
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
- SPINK4 affected M2 macrophage polarization to promote colorectal cancer malignant phenotype by PI3K/AKT pathway.BMC cancer · 2026Article
- Single-cell RNA sequencing of adenoid cystic carcinoma of the breast reveals cellular heterogeneity and tumor microenvironment features.BMC medical genomics · 2026Article
- Antigen Remodeling in Colorectal Cancer: How Radiotherapy and Chemotherapy Enhance Immunotherapy Responsiveness.Cancers · 2026Review
- Article
- Recent advances in drug repurposing for cancer immunomodulation emerging strategies, mechanistic insights, and clinical translation.Frontiers in oncology · 2026Review
- Colorectal Cancer Progression and Bone Metastasis: Molecular Mechanisms, Tumor Microenvironment, and Tumor-Bone Crosstalk.Cancer management and research · 2026Review
- Research on exosomes in cancer multidrug resistance and clinical translation.Extracellular vesicles and circulating nucleic acids · 2026Review
- Integrative single-nucleus transcriptomic analysis identifies UBE2C+ proliferative tumor cells and immune-stromal regulatory crosstalk in small cell lung cancer.Frontiers in immunology · 2026Article
- Enhancing targeted strategies for cancer immunotherapy by elucidating mRNA processing mechanisms.Frontiers in immunology · 2026Review
- Gut microbiota-innate immune crosstalk in the initiation and progression of CRC: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Extracellular vesicles cargo orchestration in colorectal cancer: immune evasion, stromal remodeling, and therapeutic frontiers.Molecular cancer · 2025Review
- Polyamine metabolism in cancer: drivers of immune evasion, ferroptosis and therapy resistance.Expert reviews in molecular medicine · 2025Review
- Integrative Single-Cell and Machine Learning Analysis Reveals Immune Microenvironment Remodelling in Lymph Node Metastasis of Lung Adenocarcinoma.Journal of cellular and molecular medicine · 2025Article
- The role of ADAR1 in human pathophysiology.Frontiers in cell and developmental biology · 2025Review
- Immunotherapy strategies targeting tumor-associated macrophages and their mechanisms of action in tumor progression.Frontiers in immunology · 2025Review
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24 authors.
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Abstract
backgroundColorectal cancer (CRC) is considered the third most common type of cancer worldwide. Tumor-associated macrophages (TAMs) have been shown to promote drug resistance. Adenosine-to-inosine RNA-editing, as regulated by adenosine deaminase acting on RNA (ADAR), is a process that induces the posttranscriptional modification of critical oncogenes. The aim of this study is to determine whether the signals from cancer cells would induce RNA-editing in macrophages.
methodsThe effects of RNA-editing on phenotypes in macrophages were analyzed using clinical samples and in vitro and in vivo models.
resultsThe intensity of the RNA-editing enzyme ADAR1 (Adenosine deaminase acting on RNA 1) in cancer and mononuclear cells indicated a strong positive correlation between the nucleus and cytoplasm. The ADAR1-positive mononuclear cells were positive for CD68 and CD163, a marker for M2 macrophages. Cancer cells transport pro-inflammatory cytokines or ADAR1 protein directly to macrophages via the exosomes, promoting RNA-editing in AZIN1 (Antizyme Inhibitor 1) and GLI1 (Glioma-Associated Oncogene Homolog 1) and resulting in M2 macrophage polarization. GLI1 RNA-editing in the macrophages induced by cancer cells promotes the secretion of SPP1, which is supplied to the cancer cells. This activates the NFκB pathway in cancer cells, promoting oxaliplatin resistance. When the JAK inhibitors were administered, oncogenic RNA-editing in the macrophages was suppressed. This altered the macrophage polarization from M2 to M1 and decreased oxaliplatin resistance in cancer cells.
conclusionsThis study revealed that ADAR1-high TAMs are crucial in regulating drug resistance in CRC and that targeting ADAR1 in TAMs could be a promising treatment approach for overcoming drug resistance in CRC.
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