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STAT1 gene deficient mice develop accelerated breast cancer growth and metastasis which is reduced by IL-17 blockade

Sanjay Varikuti1, Steve Oghumu2, Mohamad Elbaz1,3

  • 1Department of Pathology, The Ohio State University Medical Center, Columbus, Ohio, USA.

Oncoimmunology
|November 18, 2017
PubMed

Insights

Signal transducer and activator of transcription 1 (STAT1) suppresses breast cancer growth and metastasis. Blocking IL-17A in STAT1-deficient mice reduced lung metastasis, suggesting therapeutic potential.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Signal transducer and activator of transcription 1 (STAT1) is crucial for interferon-gamma signaling, influencing apoptosis, inflammation, cell cycle, and angiogenesis.
  • While STAT1's role in primary breast cancer growth is studied, its impact on metastasis is unclear.

Purpose of the Study:

  • To investigate the role of STAT1 in breast cancer metastasis using a mouse model.
  • To explore potential therapeutic strategies targeting STAT1 deficiency-related metastasis.

Main Methods:

  • Orthotopic implantation of metastatic 4T1.2 cells into wild-type (WT) or STAT1 knockout (STAT1-/-) mice.
  • Analysis of primary tumor growth, lung metastasis, myeloid-derived suppressor cell (MDSC) infiltration, and gene expression (Mmp9, Cxcl1).
  • Evaluation of anti-IL-17A treatment efficacy in STAT1-/- mice.

Main Results:

  • STAT1-/- mice exhibited faster primary tumor development, larger tumors, and increased lung metastasis compared to WT mice.
  • STAT1 deficiency led to elevated Ly6G+CD11b+ granulocytic MDSC infiltration and increased Mmp9 and Cxcl1 expression in tumors.
  • Blockade of IL-17A in STAT1-/- mice reduced MDSC accumulation and significantly decreased lung metastasis.

Conclusions:

  • STAT1 acts as a suppressor of primary breast tumor growth and metastasis.
  • Targeting IL-17A may counteract STAT1 deficiency-driven metastasis, offering a potential immunotherapy approach for immunocompromised breast cancer patients.
Keywords:
IL-17breast cancermetastasisneutrophil

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