ArticleCancer letters2021
IGFBP2 promotes tumor progression by inducing alternative polarization of macrophages in pancreatic ductal adenocarcinoma through the STAT3 pathway.
Article in Cancer letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 86 citations in OpenAlex.
- Rewiring the tumor microenvironment: IGFBP2 at the Nexus of remodeling and therapy resistance?Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Neonatal platelets differentiate monocytes to a myeloid-derived suppressor cell phenotype.Blood · 2026Article
- Hypomethylation of GNA15 Promotes Pancreatic Ductal Adenocarcinoma Progression and Macrophage M2 Polarization via STAT3-CXCL8 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- IGFBP in tumor immunity: a novel target for cancer immunotherapy.Journal of translational medicine · 2026Review
- Bidirectional Interactions Between Immune Regulation and the Insulin-like Growth Factor Axis in Colorectal Cancer.International journal of molecular sciences · 2026Review
- IGFBP2 promotes immunosuppression by regulating macrophage PD-L1 expression in NEUROD1-high small cell lung cancer.Journal of translational medicine · 2026Article
- Multifunctional nanoplatforms deciphering immune resistance in bone tumors: cooperative delivery, immune reprogramming and microenvironment remodeling.Journal of nanobiotechnology · 2026Review
- Article
- Targeting Tumor-Associated Macrophages to Reshape the Immuno-Mechanical Landscape: Molecular Mechanisms and Therapeutic Strategies.International journal of biological sciences · 2026Review
- Membrane-modified mesoporous silica nanoparticles guided by tumor immunomodulatory regulation for anti-tumor strategies.Frontiers in immunology · 2026Review
- CXCL8/SDC1 axis mediates tumor stem cell interactions to drive remote transfer in thyroid cancer.Journal of pharmaceutical analysis · 2026Article
- YTHDF3 suppresses interferon-stimulated gene (ISG)-dependent antitumor immunity and promotes HPV carcinogenesis in cervical cancer.Cell death & disease · 2025Article
- Influence of m6A regulatory factor related to immune microenvironment on the prognosis of prostate cancer.Biomedical engineering online · 2025Article
- Pathologic Signaling and Disease Implications of Insulin-like Growth Factor Binding Proteins in Cancer, Cardiovascular Disease, and Fibrosis.International journal of molecular sciences · 2025Review
- Macrophages in endometriosis: key roles and emerging therapeutic opportunities-a narrative review.Reproductive biology and endocrinology : RB&E · 2025Review
- NIPA1 depletion in tumor-associated macrophages via IGFBP2/EGFR attenuates acute myeloid leukemia progression and chemoresistance.Annals of hematology · 2025Article
- Role of m6A RNA methylation regulators in pancreatic cancer: interactions and potential implications.Cancer cell international · 2025Review
- Ginsenoside Rb1 inhibits M1 macrophages-induced IGFBP2-mediated endothelial-mesenchymal transition to alleviate myocardial fibrosis in mice with chronic heart failure.In vitro cellular & developmental biology. Animal · 2025Article
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Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Tumor-associated macrophages (TAMs) represent the M2-like phenotype with potent immunosuppressive activity, and play a pro-tumor role in pancreatic ductal adenocarcinoma (PDAC) biology. In this study, we investigated the role of the insulin-like growth factor binding protein 2 (IGFBP2) as a determinant of TAM polarity. Clinical data revealed that the levels of IGFBP2 correlated with M2 TAMs accumulation and disease progression in human PDAC. In vivo mouse model experiments showed that IGFBP2 promoted an immunosuppressive microenvironment and tumor growth in a macrophage dependent manner. Bioinformatics analysis of PDAC transcriptomes revealed a significant association between IGFBP2 expression and M2 macrophage polarization and signal transducer and activator of transcription 3 (STAT3) activation. Mechanistic investigations demonstrated that IGFBP2 augmented the expression and secretion of IL-10 through STAT3 activation in PDAC cells, which induced TAM polarization toward an M2 phenotype. IGFBP2-polarized M2 macrophages significantly increased Tregs infiltration and impaired antitumor T-cell immunity in a mouse model. Thus, our investigations have illuminated the IGFBP2 signaling pathway that contributes to the macrophage-based immunosuppressive microenvironment in PDAC, suggesting that blocking the IGFBP2 axis constitutes a potential treatment strategy to reset TAM polarization toward an antitumor state in PDAC.
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