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Hyaluronan deficiency in tumor stroma impairs macrophage trafficking and tumor neovascularization

Nobutaka Kobayashi1, Seiji Miyoshi, Takahide Mikami

  • 1Department of Molecular Oncology, Division of Molecular and Cellular Biology, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine, Nagano, Japan.

Cancer Research
|September 9, 2010
PubMed

Insights

Stromal hyaluronan (HA) is crucial for recruiting tumor-associated macrophages (TAMs) to the tumor microenvironment. This recruitment is essential for tumor angiogenesis and lymphangiogenesis, highlighting HA's role in tumor progression.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Stromal cells play a critical role in tumor progression.
  • Molecular signals regulating tumor stroma interactions are not fully understood.
  • Tumor-associated macrophages (TAMs) are key cellular components within the tumor microenvironment.

Purpose of the Study:

  • To investigate the role of stromal hyaluronan (HA) in the recruitment of TAMs.
  • To elucidate the contribution of stroma-derived HA to macrophage mobilization within tumors.
  • To examine the impact of stromal HA deficiency on tumor angiogenesis and lymphangiogenesis.

Main Methods:

  • Conditional gene targeting of the HA synthase 2 (Has2) gene in stromal fibroblasts.
  • Inoculation of Has2 null fibroblasts with tumor cells in nude mice.
  • Assessment of macrophage recruitment, tumor angiogenesis, and lymphangiogenesis.

Main Results:

  • Disruption of the Has2 gene in stromal fibroblasts significantly impaired macrophage recruitment.
  • Stroma-derived HA is essential for intratumoral macrophage mobilization.
  • Deficiency in stromal HA attenuated tumor angiogenesis and lymphangiogenesis.
  • Macrophage recruitment was impaired in conjunction with reduced angiogenesis and lymphangiogenesis.

Conclusions:

  • Stromal hyaluronan (HA) acts as a critical microenvironmental signal for recruiting TAMs.
  • TAM recruitment, mediated by stromal HA, is essential for tumor neovascularization (angiogenesis and lymphangiogenesis).
  • Targeting stromal HA production may represent a therapeutic strategy to inhibit tumor growth by modulating TAM infiltration and angiogenesis.

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