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CD47 Blockade Inhibits Tumor Progression through Promoting Phagocytosis of Tumor Cells by M2 Polarized Macrophages in

Shenglan Gu1, Ting Ni1, Jing Wang1

  • 1Department of Gynecology, International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal of Immunology Research
|December 8, 2018
PubMed

Insights

Blocking the CD47-SIRPα "don't eat me" signal enhances macrophage-mediated phagocytosis of endometrial cancer (EC) cells. This strategy inhibits tumor growth and promotes anti-tumor immunity within the tumor microenvironment (TME).

Area of Science:

  • Immunology
  • Oncology
  • Cancer Biology

Background:

  • Tumor-associated macrophages (TAMs) are increasingly targeted for cancer therapy.
  • Tumor cells use CD47 to signal macrophages via SIRPα, inhibiting phagocytosis and promoting immune evasion.
  • The role of CD47-SIRPα signaling in endometrial cancer (EC) progression and TAMs is not well understood.

Purpose of the Study:

  • To investigate the expression of CD47 in EC.
  • To elucidate the role of the CD47-SIRPα axis in TAMs and EC progression.
  • To evaluate the therapeutic potential of blocking CD47-SIRPα interaction in EC.

Main Methods:

  • Analysis of TCGA database for CD47 expression.
  • Quantitative PCR (qPCR) and flow cytometry to confirm CD47 and TAMs in EC tissues.
  • In vitro co-culture assays to assess macrophage phagocytosis of EC cells upon anti-CD47 antibody treatment.
  • In vivo studies using mouse models to evaluate tumor growth inhibition and immune cell infiltration.

Main Results:

  • Endometrial cancer tissues exhibit increased TAMs, predominantly M2 macrophages, correlating with tumor progression.
  • High CD47 expression was confirmed in EC tissues.
  • Anti-CD47 antibody treatment enhanced M2 macrophage-mediated phagocytosis of EC cells, rather than inducing direct apoptosis.
  • CD47 blockade suppressed EC tumor growth in vivo and increased the infiltration of anti-tumorigenic macrophages in the TME.

Conclusions:

  • The CD47-SIRPα pathway plays a significant role in EC progression by promoting immune evasion.
  • Blocking CD47 enhances M2 macrophage phagocytosis of EC cells and exhibits anti-tumor effects in vivo.
  • Targeting the CD47-SIRPα interaction represents a promising therapeutic strategy for endometrial cancer.

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