ArticleOncotarget2016
TGF-β induces M2-like macrophage polarization via SNAIL-mediated suppression of a pro-inflammatory phenotype.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 377 papers, 1 of them a synthesis that pooled it.
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Who cites it
377 citing papers in PubMed, 1 synthesis or guideline pooled it, 547 citations in OpenAlex.
- Signaling pathway mechanisms in pancreatic ductal adenocarcinoma tumor microenvironment and emerging targeting strategies for improved prognosis.Oncology reviews · 2026Pooled it
- Polarization of tumor-infiltrating macrophages predicts complete response to neoadjuvant treatment in patients with rectal cancer.Oncoimmunology · 2026Article
- Growth factor applications and clinical translation: advances and challenges.Annals of medicine · 2026Review
- Epithelial to mesenchymal transition and M2 macrophages drive aggressiveness in murine and human sarcomatoid urothelial carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Sulf1 regulates inflammation via modulation of TGF-β dependent epicardial activation.EMBO reports · 2026Article
- Beyond immunity: macrophage plasticity in vascular regeneration.npj biomedical innovations · 2026Review
- Integrated multi-omics identifies lineage-dependent myeloid cells recruitment and the APP-CD74 axis as an immunoregulatory target in pediatric high-grade glioma.Acta neuropathologica · 2026Article
- Immunotherapy Rechallenge in HCC: A Second Chance for Response?Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- Review
- Tissue-specific matrix-bound nanovesicles regulate the immunoregulatory progress of biological mesh-aided abdominal hernia repair.Bioactive materials · 2026Article
- ACKR2 aids the regulation of bone marrow eosinophils to promote monocyte differentiation and anti-bacterial immunity.Nature communications · 2026Article
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Postpartum breast cancer as a distinct oncologic entity: linking physiological tissue remodelling to tumor biology and clinical translation.Breast cancer research : BCR · 2026Review
- M2 Macrophage Polarization Characterizes an Immunosuppressive Microenvironment in Extracranial Arteriovenous Malformations.Biomedicines · 2026Article
- Tuberculosis and Cellular Metabolism: Insights into the Crosstalk Between Macrophage Immunometabolism and Muscle Dysregulation.International journal of molecular sciences · 2026Review
- GM-CSF downregulates type I IFN responses in glioblastoma-associated monocytes.Experimental & molecular medicine · 2026Article
- Divergent macrophage-regulated T cell states determine response to Bacillus Calmette-Guérin vaccine in high-risk bladder cancer.The Journal of clinical investigation · 2026Article
- Tailored Porous Bimetallic Nanozyme Platform for Full-Cycle Therapeutics of Intestinal Ischemia/Reperfusion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease.Cells · 2026Review
317 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated macrophages (TAMs) are a major component of leukocytic infiltrate in tumors, which facilitates tumor progression and promotes inflammation. TGF-β promotes the differentiation of non-activated macrophages into a TAM-like (M2-like) phenotype; however, the underlying mechanisms are not clear. In this study, we found that TGF-β induces a M2-like phenotype characterized by up-regulation of the anti-inflammatory cytokine IL-10, and down-regulation of the pro-inflammatory cytokines TNF-α and IL-12. In human THP-1 macrophages, overexpression of SNAIL caused M2-like differentiation by inhibiting pro-inflammatory cytokine release and promoting the expression of M2-specific markers. By contrast, SNAIL knockdown promoted M1 polarization through up-regulation of pro-inflammatory cytokines and abolished TGF-β-mediated M2-polarization of THP-1 macrophages. The SMAD2/3 and PI3K/AKT signaling pathways were crucial for TGF-β-induced SNAIL overexpression in THP-1 cells. These findings suggest that TGF-β skews macrophage polarization towards a M2-like phenotype via SNAIL up-regulation, and blockade of TGF-β/SNAIL signaling restores the production of pro-inflammatory cytokines. This study provides new understanding of the role of SNAIL in M2 polarization of macrophages, and suggests a potential therapeutic target for antitumor immunity.
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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.