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STAT3/HOTAIR Signaling Axis Regulates HNSCC Growth in an EZH2-dependent Manner

Shanshan Sun1,2, Yansheng Wu1, Wenyu Guo1

  • 1Department of Maxillofacial and Otorhinolaryngology Oncology, Tianjin Medical University Cancer Institute and Hospital, Key Laboratory of Cancer Prevention and Therapy, Tianjin Cancer Institute, National Clinical Research Center of Cancer, Tianjin, China.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|March 16, 2018
PubMed

Insights

STAT3 signaling promotes head and neck cancer (HNSCC) growth by regulating HOTAIR and pEZH2-S21. Targeting this axis may improve HNSCC treatment sensitivity to therapies like cisplatin and cetuximab.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Phosphoinositide 3-kinase (PI3K) and Signal transducer and activator of transcription 3 (STAT3) are frequently activated during cancer progression.
  • The long non-coding RNA HOX transcript antisense RNA (HOTAIR) is implicated in modulating head and neck squamous cell cancer (HNSCC) progression.

Purpose of the Study:

  • To investigate the correlation between PI3K/STAT3/HOTAIR signaling and HNSCC progression.
  • To determine the impact of this signaling pathway on HNSCC sensitivity to platinum-based and anti-EGFR targeted therapies.

Main Methods:

  • Analysis of STAT3, HOTAIR, PI3K, and AKT levels in human HNSCC samples.
  • In vitro and in vivo experiments involving activation or suppression of STAT3/HOTAIR.
  • Assessment of HNSCC cell sensitivity to cisplatin and cetuximab.

Main Results:

  • Significantly elevated expression/activation of STAT3, HOTAIR, PI3K, and AKT was observed in HNSCC samples compared to normal tissue.
  • STAT3 inhibition reduced HOTAIR levels and increased HNSCC sensitivity to cisplatin and cetuximab.
  • STAT3 promotes HOTAIR transcription and its interaction with pEZH2-S21, enhancing HNSCC growth; HOTAIR overexpression accelerated tumor growth in vivo.

Conclusions:

  • STAT3 signaling drives HNSCC progression by regulating HOTAIR and pEZH2-S21 in the context of PI3K activation.
  • The STAT3/HOTAIR/pEZH2-S21 axis represents a potential therapeutic target for HNSCC treatment.

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