ArticleMedical science monitor basic research2017
M3 Macrophages Stop Division of Tumor Cells In Vitro and Extend Survival of Mice with Ehrlich Ascites Carcinoma.
Article in Medical science monitor basic research, 2017. 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, 32 citations in OpenAlex.
- Phenotypic switching of gastrointestinal smooth muscle cells and the regulatory role of macrophages: a literature review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Article
- Epigenetic programming of macrophages across inflammatory and malignant diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Antitumor efficacy of intermittent low-dose erlotinib plus sulindac via MHC upregulation and remodeling of the immune cell niche.International journal of cancer · 2025Article
- Breast Cancer and Tumor Microenvironment: The Crucial Role of Immune Cells.Current oncology (Toronto, Ont.) · 2025Review
- Article
- Interleukin-27-polarized HIV-resistant M2 macrophages are a novel subtype of macrophages that express distinct antiviral gene profiles in individual cells: implication for the antiviral effect via different mechanisms in the individual cell-dependent manner.Frontiers in immunology · 2025Article
- CXCL4 deficiency limits M4 macrophage infiltration and attenuates hyperoxia-induced lung injury.Molecular medicine (Cambridge, Mass.) · 2024Article
- Reprogramming of breast tumor-associated macrophages with modulation of arginine metabolism.Life science alliance · 2024Article
- Cystatin M/E ameliorates bone resorption through increasing osteoclastic cell estrogen influx.Research square · 2024Article
- Macrophages, Metabolism, Mitochondria, Circadian Rhythmicity and the Pathogen: The Multidimensional Nature of Tuberculosis.Results and problems in cell differentiation · 2024Review
- Cholinergic Polarization of Human Macrophages.International journal of molecular sciences · 2023Review
- Reprogramming of breast tumor-associated macrophages with modulation of arginine metabolism.bioRxiv : the preprint server for biology · 2023Article
- Recent insight into the role of macrophage in alcohol-associated liver disease: a mini-review.Frontiers in cell and developmental biology · 2023Review
- Review
- A vicious circle in breast cancer: The interplay between inflammation, reactive oxygen species, and microRNAs.Frontiers in oncology · 2022Review
- Progress of the Art of Macrophage Polarization and Different Subtypes in Mycobacterial Infection.Frontiers in immunology · 2021Review
- CD163 as a Biomarker in Colorectal Cancer: The Expression on Circulating Monocytes and Tumor-Associated Macrophages, and the Soluble Form in the Blood.International journal of molecular sciences · 2020Article
- Role of Macrophages in the Progression and Regression of Vascular Calcification.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND M1 macrophages target tumor cells. However, many tumors produce anti-inflammatory cytokines, which reprogram the anti-tumor M1 macrophages into the pro-tumor M2 macrophages. We have hypothesized that the problem of pro-tumor macrophage reprogramming could be solved by using a special M3 switch phenotype. The M3 macrophages, in contrast to the M1 macrophages, should respond to anti-inflammatory cytokines by increasing production of pro-inflammatory cytokines to retain its anti-tumor properties. Objectives of the study were to form an M3 switch phenotype in vitro and to evaluate the effect of M3 macrophages on growth of Ehrlich ascites carcinoma (EAC) in vitro and in vivo. MATERIAL AND METHODS Tumor growth was initiated by an intraperitoneal injection of EAC cells into C57BL/6J mice. RESULTS 1) The M3 switch phenotype can be programed by activation of M1-reprogramming pathways with simultaneous inhibition of the M2 phenotype transcription factors, STAT3, STAT6, and/or SMAD3. 2) M3 macrophages exerted an anti-tumor effect both in vitro and in vivo, which was superior to anti-tumor effects of cisplatin or M1 macrophages. 3) The anti-tumor effect of M3 macrophages was due to their anti-proliferative effect. CONCLUSIONS Development of new biotechnologies for restriction of tumor growth using in vitro reprogrammed M3 macrophages is very promising.
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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.