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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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HOXC11 promotes head and neck squamous cell carcinomas (HNSCC) progression by regulating SPHK1 through the Wnt

Jing Zhang1,2,3, Qionghui Wu1,2,3, Jingyuan Liu1,2,3

  • 1Department of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Cancer Gene Therapy
|July 25, 2026
PubMed

Insights

HOXC11 promotes head and neck squamous cell carcinoma (HNSCC) progression by regulating SPHK1 via the Wnt/β-catenin pathway. Silencing HOXC11 inhibits HNSCC tumor growth, revealing a new therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • Head and neck squamous cell carcinomas (HNSCC) require novel therapeutic targets.
  • Understanding molecular mechanisms driving HNSCC progression is critical.

Purpose of the Study:

  • To investigate the roles of HOXC11 and SPHK1 in HNSCC.
  • To elucidate the involvement of the Wnt signaling pathway in HNSCC pathogenesis.
  • To identify a novel regulatory axis in HNSCC.

Main Methods:

  • Utilized HNSCC cell lines (FaDu, SCC-15) and a xenograft model.
  • Employed quantitative PCR (qPCR) and Western Blotting (WB) for gene and protein analysis.
  • Assessed cell proliferation, migration, invasion, and apoptosis using colony formation, Transwell assays, wound healing, and flow cytometry.

Main Results:

  • HOXC11 and SPHK1 were highly expressed in HNSCC and linked to the Wnt pathway.
  • HOXC11 promoted proliferation, migration, invasion, and inhibited apoptosis in HNSCC.
  • SPHK1 silencing impaired HNSCC progression and altered Wnt signaling; its overexpression reversed HOXC11 knockdown effects.
  • HOXC11 promotes HNSCC progression by upregulating SPHK1 via the Wnt/β-catenin pathway.

Conclusions:

  • HOXC11 drives HNSCC progression through the HOXC11/SPHK1/Wnt/β-catenin axis.
  • Targeting HOXC11 presents a potential therapeutic strategy for HNSCC.
  • This study identifies a novel regulatory mechanism in HNSCC development.

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