ArticleCell communication and signaling : CCS2022
Tumor-associated macrophages promote epithelial-mesenchymal transition and the cancer stem cell properties in triple-negative breast cancer through CCL2/AKT/β-catenin signaling.
Article in Cell communication and signaling : CCS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
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Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- From tumor microenvironment orchestrators to actionable targets: a systematic review of TAM-targeted therapies in triple-negative breast cancer.International journal of clinical oncology · 2026Pooled it
- Multi-platform analysis of the tumor immune microenvironment associated with breast cancer subtypes.Oncoimmunology · 2026Article
- Nanotechnology-enabled precision targeting of lung cancer stem cells: Recent developments and therapeutic implications.Stem cell reviews and reports · 2026Review
- Translational insights and clinical challenges of targeting cancer stem cells.Signal transduction and targeted therapy · 2026Review
- Cancer stem cells and drug resistance in cancer: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Serum CCL2 and CCL7 in Prostate Cancer: Evaluation of Their Diagnostic Utility in Comparison with Benign Prostatic Hyperplasia and Healthy Controls.International journal of molecular sciences · 2026Article
- Hippo pathway at the crossroads of stemness and therapeutic resistance in breast cancer.Molecular oncology · 2026Review
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- PFAS is associated with perineural invasion in triple-negative breast cancer with a potential role for Cathepsin D dysregulation: a multi-omics and experimental study.Clinical and experimental medicine · 2026Article
- TCF12-mediated transcriptional activation of CCDC34 is involved in the positive feedback of tumor-associated macrophages and EMT to promote LUSC.Cell biology and toxicology · 2026Article
- Research progress and trends on M2 macrophages in breast cancer research: a bibliometric analysis.Discover oncology · 2026Article
- Article
- MLK4 orchestrates macrophage-induced triple-negative breast cancer invasion and ECM remodeling via enhanced paracrine signaling and NF-κB-MMP axis activation.Cell death & disease · 2026Article
- From Signaling Pathways to Combination Therapy: Bioactive Compounds against Cancer Stem Cells.Stem cell reviews and reports · 2026Review
- Allogeneic Immune Cell Perfusion Inhibits the Growth of Vascularized 3D In Vitro Tumor Models, Induces Vascular Regression and Desmoplasia, but Promotes Tumor Cell Invasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- DCC-2036 induces repolarization of TAMs to M1 type and enhances CD8Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Fibronectin Is a Likely Therapeutic Target Shared by Oral and Breast Carcinomas.International journal of molecular sciences · 2026Article
- The puppet master in the breast cancer "microecological community": spatial and metabolic regulation of macrophage heterogeneity.Molecular cancer · 2026Review
- The chemokine network in triple-negative breast cancer: its role in immune microenvironment regulation, and prospects for targeted therapy.Frontiers in immunology · 2026Review
- Astragaloside IV in hepatocellular carcinoma: repolarizing macrophages to reprogram the tumor microenvironment.Frontiers in pharmacology · 2026Review
47 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTriple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer with poor prognosis and limited treatment. As a major component of the tumor microenvironment, tumor-associated macrophages (TAMs) play an important role in facilitating the aggressive behavior of TNBC. This study aimed to explore the novel mechanism of TAMs in the regulation of epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) properties in TNBC.
methodsExpression of the M2-like macrophage marker CD163 was evaluated by immunohistochemistry in human breast cancer tissues. The phenotype of M2 macrophages polarized from Tohoku-Hospital-Pediatrics-1 (THP1) cells was verified by flow cytometry. Transwell assays, wound healing assays, western blotting, flow cytometry, ELISA, quantitative polymerase chain reaction (qPCR), luciferase reporter gene assays, and immunofluorescence assays were conducted to investigate the mechanism by which TAMs regulate EMT and CSC properties in BT549 and HCC1937 cells.
resultsClinically, we observed a high infiltration of M2-like tumor-associated macrophages in TNBC tissues and confirmed that TAMs were associated with unfavorable prognosis in TNBC patients. Moreover, we found that conditioned medium from M2 macrophages (M2-CM) markedly promoted EMT and CSC properties in BT549 and HCC1937 cells. Mechanistically, we demonstrated that chemokine (C-C motif) ligand 2 (CCL2) secretion by TAMs activated Akt signaling, which in turn increased the expression and nuclear localization of β-catenin. Furthermore, β-catenin knockdown reversed TAM-induced EMT and CSC properties.
conclusionsThis study provides a novel mechanism by which TAMs promote EMT and enhance CSC properties in TNBC via activation of CCL2/AKT/β-catenin signaling, which may offer new strategies for the diagnosis and treatment of TNBC. Video Abstract.
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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.