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Updated: Jun 29, 2025

Studying the Effects of Tumor-Secreted Paracrine Ligands on Macrophage Activation using Co-Culture with Permeable Membrane Supports
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[Tumor-associated Macrophage: 
Emerging Targets for Modulating the Tumor Microenvironment]

Yinxue Zhou1, Dunqiang Ren1, Huanhuan Bi2

  • 1Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Qingdao University, Qingdao 266000, China.

Zhongguo Fei AI Za Zhi = Chinese Journal of Lung Cancer
|April 9, 2024
PubMed

Insights

Tumor-associated macrophages (TAM) drive lung cancer progression by creating an immunosuppressive environment. Anti-angiogenic drugs show potential in reprogramming these pro-tumor TAM into anti-tumor cells, offering new therapeutic strategies.

Area of Science:

  • Oncology
  • Immunology
  • Cancer Biology

Background:

  • Tumor-associated macrophages (TAM) are key regulators of the lung cancer immune microenvironment.
  • TAM influence tumor initiation, progression, invasion, and metastasis through phenotypic and functional changes.
  • Macrophages polarize into M1 (anti-tumor) and M2 (pro-tumor) subtypes; TAM typically adopt the M2 phenotype, suppressing anti-tumor immunity.

Approach:

  • This review examines the role of anti-angiogenic drugs in modulating TAM phenotypes.
  • Focuses on the potential of these drugs to reprogram M2 TAM towards an M1 phenotype.
  • Discusses the implications of TAM functional alterations in anti-angiogenic and immunotherapy.

Key Points:

  • TAM polarization into the M2 phenotype promotes immune suppression and tumor growth in lung cancer.
  • Anti-angiogenic therapies can potentially reverse M2 TAM polarization to an anti-tumor M1 state.
  • TAM function is critical for the efficacy of both anti-angiogenic therapy and immunotherapy.

Conclusions:

  • Modulating TAM polarization and function presents novel therapeutic targets for lung cancer.
  • Reprogramming TAM offers a promising strategy for enhancing anti-tumor immunity and treatment outcomes.
  • Targeting TAM may overcome resistance and improve the effectiveness of current lung cancer therapies.
Keywords:
Anti-angiogenic therapyLung neoplasmsPolarizationTumor-associated macrophage

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