ArticleOncogene2011
Pleiotropic regulation of macrophage polarization and tumorigenesis by formyl peptide receptor-2.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 105 papers.
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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
105 citing papers in PubMed, 185 citations in OpenAlex.
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- Myeloid landscape profiling identifies DLBCL-specific suppressive macrophages colocalized with blood endothelial cells.Blood advances · 2026Article
- The paracrine effects of tumor cells on endothelial cells and macrophages in brain metastases with different primary sites.Frontiers in immunology · 2026Article
- Article
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- Serum amyloid A: multifaceted roles in inflammation and cellular interactions.Immunologic research · 2025Review
- USP7 at the Crossroads of Ubiquitin Signaling, Cell Cycle, and Tumorigenesis.Molecules (Basel, Switzerland) · 2025Review
- KC1036, a multi-kinase inhibitor with anti-angiogenic activity, can effectively suppress the tumor growth of Ewing sarcoma.Angiogenesis · 2025Article
- Dual roles and therapeutic targeting of tumor-associated macrophages in tumor microenvironments.Signal transduction and targeted therapy · 2025Review
- The landscape of malignant transition: Unraveling cancer cell-of-origin and heterogeneous tissue microenvironment.Cancer letters · 2025Article
- Functional Interactions Between Recombinant Serum Amyloid A1 (SAA1) and Chemokines in Leukocyte Recruitment.International journal of molecular sciences · 2025Review
- Human antimicrobial/host defense peptide LL-37 may prevent the spread of a local infection through multiple mechanisms: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Inosine Prevents Colorectal Cancer Progression by Inducing M1 Phenotypic Polarization of Macrophages.Molecules (Basel, Switzerland) · 2024Article
- Dissection of pro-tumoral macrophage subtypes and immunosuppressive cells participating in M2 polarization.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Review
- An overview of the regulatory role of annexin A1 in the tumor microenvironment and its prospective clinical application (Review).International journal of oncology · 2024Review
- Single-cell Landscape of Malignant Transition: Unraveling Cancer Cell-of-Origin and Heterogeneous Tissue Microenvironment.Research square · 2024Article
- Loss of Endothelial Annexin A1 Aggravates Inflammation-Induched Vascular Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Circulating Exosomes from Septic Mice Activate NF-κB/MIR17HG Pathway in Macrophages.Biomedicines · 2024Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells recruit monocytes, macrophages and other inflammatory cells by producing abundant chemoattractants and growth factors, such as macrophage colony-stimulating factor (M-CSF/CSF-1) and monocyte chemoattractant protein-1 (MCP-1/CCL2), to promote tumor growth and dissemination. An understanding of the mechanisms that target cancer cells and regulate tumor microenvironment is essential in designing anticancer therapies. Here, we showed that serum amyloid-A (SAA) and cathelicidin (LL-37) stimulated M-CSF and MCP-1 expression with or without lipopolysaccharide (LPS) administration; conversely, lipoxin-A(4) (LXA(4)) and annexin-A1 (ANXA1) inhibited LPS-induced M-CSF and MCP-1 production by human (HepG2) and mouse (H22) hepatocellular carcinoma cells (HCCs). The effects of LXA(4), ANXA1, SAA and LL-37 were dependent on the activation of their mutual cell-surface receptor formyl peptide receptor-2 (FPR2) and subsequent ROS-MAPK-NF-kB signalings. Furthermore, our results indicated that LPS switched macrophages into an IL-10(low)IL-12(high) M1 profile, whereas M-CSF+MCP-1 and FPR2 agonists skewed them into M2 (IL-10(high)IL-12(low)). In that respect, through modulating the phosphorylation of signal transducer and activator of transcription-3 (STAT3), LXA(4) and ANXA1 induced monocyte differentiation into M2a+M2c-like cells and showed antitumorigenetic activities, whereas SAA, LL-37 and M-CSF+MCP-1 led to M2b- or M2d-like polarization, which exacerbated HCC invasion in vitro and in vivo, respectively. Our results suggest that FPR2 has an appreciable pleiotropic regulator role in tumor immunoediting.
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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.