ArticlePloS one2014
Rac2 controls tumor growth, metastasis and M1-M2 macrophage differentiation in vivo.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
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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
81 citing papers in PubMed, 124 citations in OpenAlex.
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- Potential applications of gene expression profiles obtained from circulating extracellular vesicles in breast cancer.The journal of liquid biopsy · 2025Article
- Real-time imaging reveals a role for macrophage protrusive motility in melanoma invasion.The Journal of cell biology · 2025Article
- The Molecular Mechanism of Macrophages in Response to Mechanical Stress.Annals of biomedical engineering · 2025Review
- Long-term hyperglycaemia exerts contrasting effects on M1- and M2-like macrophages.Frontiers in immunology · 2025Article
- New insights into SYK targeting in solid tumors.Trends in pharmacological sciences · 2024Review
- Key Disease-Related Genes and Immune Cell Infiltration Landscape in Inflammatory Bowel Disease: A Bioinformatics Investigation.International journal of molecular sciences · 2024Article
- Harnessing the potential of monocytes/macrophages to regenerate tissue-engineered vascular grafts.Cardiovascular research · 2024Review
- The role of MAPK, notch and Wnt signaling pathways in papillary thyroid cancer: Evidence from a systematic review and meta-analyzing microarray datasets employing bioinformatics knowledge and literature.Biochemistry and biophysics reports · 2024Article
- Article
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- Macrophages inhibit extracellular hyphal growth ofInfection and immunity · 2024Article
- Research progress on the correlation between platelet aggregation and tumor progression.Histology and histopathology · 2024Review
- Migration, invasion, and metastasis are mediated byFrontiers in oncology · 2024Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Although it is well-established that the macrophage M1 to M2 transition plays a role in tumor progression, the molecular basis for this process remains incompletely understood. Herein, we demonstrate that the small GTPase, Rac2 controls macrophage M1 to M2 differentiation and the metastatic phenotype in vivo. Using a genetic approach, combined with syngeneic and orthotopic tumor models we demonstrate that Rac2-/- mice display a marked defect in tumor growth, angiogenesis and metastasis. Microarray, RT-PCR and metabolomic analysis on bone marrow derived macrophages isolated from the Rac2-/- mice identify an important role for Rac2 in M2 macrophage differentiation. Furthermore, we define a novel molecular mechanism by which signals transmitted from the extracellular matrix via the α4β1 integrin and MCSF receptor lead to the activation of Rac2 and potentially regulate macrophage M2 differentiation. Collectively, our findings demonstrate a macrophage autonomous process by which the Rac2 GTPase is activated downstream of the α4β1 integrin and the MCSF receptor to control tumor growth, metastasis and macrophage differentiation into the M2 phenotype. Finally, using gene expression and metabolomic data from our Rac2-/- model, and information related to M1-M2 macrophage differentiation curated from the literature we executed a systems biologic analysis of hierarchical protein-protein interaction networks in an effort to develop an iterative interactome map which will predict additional mechanisms by which Rac2 may coordinately control macrophage M1 to M2 differentiation and metastasis.
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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.