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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Related Experiment Video

Updated: Feb 28, 2026

Intramucosal Inoculation of Squamous Cell Carcinoma Cells in Mice for Tumor Immune Profiling and Treatment Response Assessment
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STAT3 Induces Immunosuppression by Upregulating PD-1/PD-L1 in HNSCC.

L L Bu1,2, G T Yu1, L Wu1

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

Journal of Dental Research
|June 13, 2017
PubMed
Summary

Signal transducer and activator of transcription 3 (STAT3) signaling promotes programmed death-1 (PD-1) and its ligand (PD-L1) expression in head and neck squamous cell carcinoma (HNSCC). Targeting STAT3 may enhance immunotherapy for HNSCC.

Keywords:
S3I-201cytokineimmune checkpointimmune escapeimmunotherapymice model

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Head and neck squamous cell carcinoma (HNSCC) is a prevalent cancer with ongoing advances in immunotherapy.
  • Immune checkpoint inhibitors targeting programmed death 1 (PD-1) and its ligand (PD-L1) show promise, but their regulatory mechanisms in HNSCC require further elucidation.
  • Understanding the molecular pathways that control PD-1/PD-L1 expression is crucial for optimizing HNSCC immunotherapy.

Purpose of the Study:

  • To investigate the role of signal transducer and activator of transcription 3 (STAT3) activation in regulating PD-1 and PD-L1 expression in HNSCC.
  • To explore the correlation between phosphorylated STAT3 (p-STAT3) and PD-1/PD-L1 levels in HNSCC.
  • To assess the therapeutic potential of targeting STAT3 signaling for HNSCC treatment.

Main Methods:

  • Immunostaining was employed to analyze the expression and correlation of p-STAT3 with PD-1/PD-L1 in human and mouse HNSCC tissue sections.
  • A small molecule inhibitor was used to target STAT3 in the CAL27 HNSCC cell line.
  • STAT3 signaling blockade was evaluated in a Tgfbr1/Pten 2cKO HNSCC mouse model.

Main Results:

  • Overexpression of PD-1 and PD-L1 was significantly associated with p-STAT3 in both human and mouse HNSCC.
  • Inhibition of STAT3 using a small molecule effectively reduced PD-L1 expression in the CAL27 cell line.
  • Blocking STAT3 signaling led to the downregulation of PD-1/PD-L1 in a preclinical HNSCC mouse model.

Conclusions:

  • STAT3 signaling plays a significant role in the regulation of PD-1/PD-L1 expression in HNSCC.
  • Targeting STAT3 represents a potential strategy to enhance antitumor immune responses in HNSCC.
  • These findings provide insights into the molecular mechanisms underlying immunotherapy resistance and suggest novel therapeutic avenues for HNSCC.