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Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
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Targeting phosphorylation of STAT3 delays tumor growth in HPV-negative anal squamous cell carcinoma mouse model

Lin-Lin Bu1,2, Yi-Cun Li1, Guang-Tao Yu1

  • 1The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, 430079, China.

Scientific Reports
|July 28, 2017
PubMed

Insights

Signal transducer and activation of transcription 3 (STAT3) inhibition with S3I-201 shows anti-tumor effects in a mouse model of human papillomavirus-negative anal squamous cell carcinoma (ASCC). This approach reduced tumor growth and altered the tumor immune microenvironment.

Area of Science:

  • Oncology
  • Immunology
  • Pharmacology

Background:

  • Human papillomavirus-negative anal squamous cell carcinoma (ASCC) exhibits poor response to conventional chemoradiotherapy.
  • Signal transducer and activation of transcription 3 (STAT3) is hyper-activated in HPV-negative ASCC.
  • Novel therapeutic strategies are needed for this patient population.

Purpose of the Study:

  • To investigate the therapeutic potential of STAT3 inhibition using S3I-201 in an HPV-negative ASCC mouse model.
  • To evaluate the effects of S3I-201 on tumor growth, cancer cell biomarkers, and the tumor immune microenvironment.

Main Methods:

  • In vivo administration of S3I-201 to an established HPV-negative ASCC mouse model.
  • Tumor growth and burden assessment.
  • Analysis of biomarkers (survivin, Ki67) using immunohistochemistry.
  • Flow cytometry and immunohistofluorescence assays to quantify immune cell populations (MDSCs, TAMs).

Main Results:

  • S3I-201 treatment significantly delayed tumor growth, resulting in smaller tumor size and burden compared to controls.
  • Survivin and Ki67 expression were significantly reduced in the S3I-201 treatment group.
  • S3I-201 treatment led to decreased populations of myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs).
  • These findings suggest a reversion of the immunosuppressive tumor microenvironment.

Conclusions:

  • S3I-201 demonstrates significant anti-tumor effects in an HPV-negative ASCC mouse model.
  • STAT3 inhibition impacts both cancer cell proliferation/survival and the tumor immune landscape.
  • S3I-201 represents a potential novel therapeutic strategy for HPV-negative ASCC.

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