Related Experiment Video
Updated: Feb 24, 2026

In Vitro Assay to Study Tumor-macrophage Interaction
Published on: August 1, 2019
Diversity and function of tumor-associated macrophages in brain metastases: mechanisms and therapeutic prospects
Yingping Ma1, Hongyu Wang1, Xinman Dou2
1Department of Neurosurgery, The Second Hospital of Lanzhou University, Lanzhou, China.
Abstract:
Brain metastasis significantly worsens prognosis in late-stage cancer., with Its treatment hindered by the blood-brain barrier (BBB) and an immunosuppressive tumor microenvironment. Within this environment, tumor-associated macrophages (TAMs) represent the predominant immune population. Through their roles in immune modulation, angiogenesis, and tumor invasion, TAMs are critical drivers of disease progression. TAMs are highly heterogeneous. While traditionally categorized into M1 (anti-tumor) or M2 (pro-tumor) phenotypes, this dichotomy is an oversimplification. Recent single-cell studies have revealed a spectrum of functional subpopulations, such as lipid-associated, interferon-responsive, and pro-angiogenic TAMs, with M2-like states typically prevailing to mediate immunosuppression. This review explores the diversity and functions of TAMs in brain metastasis. We first detail their biological characteristics, including origins, heterogeneous subtype classifications (e.g., lipid-associated macrophages that extend beyond the simple M1/M2 dichotomy), and polarization states. We further discuss how polarization is regulated by signaling pathways (e.g., STAT, NF-κB) and microenvironmental factors (e.g., hypoxia, metabolic reprogramming). We examine TAM roles from pre-metastatic niche formation to tumor colonization, using breast and lung cancer brain metastases to illustrate how TAMs disrupt the BBB and facilitate immune evasion through molecules like ANGPTL4 (angiopoietin-like 4) and MMP9. Key pathways of TAM-tumor cell interactions, including neuro-cancer interactions, immune-metabolic regulation, and exosome-mediated communication, are also discussed. Targeting TAMs offers promising therapeutic avenues. These strategies include reprogramming TAMs (e.g., using CSF1R inhibitors), combining TAM-targeted therapy with immune checkpoint inhibitors, and developing novel approaches such as nanotechnology and CAR-macrophages. However, several challenges remain, including TAM heterogeneity, lack of targeting specificity, and the obstacle of BBB delivery. Future research should leverage technologies like single-cell sequencing and spatial transcriptomics to decode TAM heterogeneity, and develop personalized treatments based on biomarkers such as GPNMB and TRAIL, aiming to improve patient outcomes in brain metastasis.
Insights
Tumor-associated macrophages (TAMs) drive brain metastasis by disrupting the blood-brain barrier and suppressing immunity. Targeting TAM heterogeneity offers new therapeutic strategies for brain cancers, despite challenges in delivery and specificity.
Area of Science:
- Oncology
- Immunology
- Neuroscience
Background:
- Brain metastasis significantly worsens cancer prognosis, with treatment challenged by the blood-brain barrier (BBB) and immunosuppressive tumor microenvironment.
- Tumor-associated macrophages (TAMs) are the predominant immune cells in this environment, driving disease progression through immune modulation, angiogenesis, and invasion.
- TAMs exhibit significant heterogeneity, extending beyond the simplified M1/M2 classification to include diverse functional subpopulations.
Purpose of the Study:
- To explore the diversity and functions of TAMs in brain metastasis.
- To detail TAM biological characteristics, polarization regulation, and roles in disease progression.
- To discuss current and future therapeutic strategies targeting TAMs for brain metastasis.
Main Methods:
- Review of literature on TAM biology, polarization, and function in brain metastasis.
- Analysis of TAM roles in pre-metastatic niche formation, BBB disruption, and immune evasion.
- Examination of therapeutic strategies including TAM reprogramming, combination therapies, and novel approaches.
Main Results:
- TAMs, particularly M2-like phenotypes, mediate immunosuppression and facilitate brain metastasis progression.
- TAMs disrupt the BBB and promote immune evasion via molecules like ANGPTL4 and MMP9.
- Key TAM-tumor cell interactions involve neuro-cancer signaling, immune-metabolic regulation, and exosome communication.
Conclusions:
- Targeting TAMs presents promising therapeutic avenues for brain metastasis, including reprogramming and combination therapies.
- Challenges remain in addressing TAM heterogeneity, targeting specificity, and BBB drug delivery.
- Future research should utilize advanced technologies to decode TAM heterogeneity and develop personalized, biomarker-driven treatments.
More Related Videos
Related Concept Videos
The Tumor Microenvironment
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Mesenchymal Stem Cells

