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Targeting STAT3 signaling reduces immunosuppressive myeloid cells in head and neck squamous cell carcinoma

Lin-Lin Bu1, Guang-Tao Yu2, Wei-Wei Deng2

  • 1The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine, Ministry of Education, Wuhan, China; Department of Oral Maxillofacial-Head Neck Oncology, School and Hospital of Stomatology, Wuhan University, Wuhan, China.

Oncoimmunology
|July 29, 2016
PubMed

Insights

Inhibiting signal transducer and activator of transcription 3 (STAT3) may enhance antitumor immunity. Targeting STAT3 with S3I-201 reduced immunosuppressive myeloid cells, including myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs), in head and neck squamous cell carcinoma (HNSCC).

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Constitutively activated signal transducer and activator of transcription 3 (STAT3) signaling is implicated in immune suppression within the tumor microenvironment.
  • STAT3 activation is linked to the presence of immunosuppressive myeloid cells, such as myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs).
  • Targeting STAT3 is a potential therapeutic strategy to enhance antitumor immunity in various cancers, including head and neck squamous cell carcinoma (HNSCC).

Purpose of the Study:

  • To investigate the association between phosphorylated STAT3 levels and the abundance of MDSCs and TAMs in human HNSCC.
  • To evaluate the efficacy of a selective STAT3 inhibitor, S3I-201, in reducing immunosuppressive myeloid cells in a preclinical HNSCC model.

Main Methods:

  • Analysis of phosphorylated STAT3 levels and markers for MDSCs and TAMs in human HNSCC tissues.
  • Administration of the selective STAT3 inhibitor S3I-201 to a genetically defined mouse model of HNSCC.
  • Assessment of changes in immature myeloid cells (MDSCs, TAMs, iDCs) following S3I-201 treatment.

Main Results:

  • High levels of phosphorylated STAT3 were significantly correlated with increased MDSCs and TAMs in human HNSCC.
  • Treatment with S3I-201 led to a significant decrease in immature myeloid cells, including MDSCs, TAMs, and immature dendritic cells (iDCs), in the mouse HNSCC model.
  • These findings suggest a role for STAT3 in regulating immunosuppressive myeloid cell populations in HNSCC.

Conclusions:

  • Targeting STAT3 signaling with S3I-201 demonstrates potential for enhancing antitumor immunity in HNSCC.
  • Inhibition of STAT3 may be an effective strategy to reduce immunosuppressive myeloid cells, thereby improving the anti-cancer immune response.
  • Further investigation into STAT3 inhibition as a therapeutic approach for HNSCC is warranted.
Keywords:
Head and neck squamous cell carcinomaSTAT3myeloid-derived suppressor cellstumor-associated macrophages

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