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<p>The discovery of potential targets in Head and neck squamous cell carcinomas (HNSCC) through molecular and mechanism analyses is crucial for understanding and treating this disease. This study utilized rigorous methods, including cell lines (FaDu and SCC-15) and a xenograft tumor model. Transfections were conducted using the Lipofectamine 2000 kit, and the evaluation of HOXC11, SPHK1, apoptosis-related protein, and the Wnt signaling pathway was carried out using qPCR and WB methods. The cell proliferation, migration, invasion, and apoptosis were comprehensively evaluated using colony formation, Transwell, wound healing, and flow cytometry, respectively. HOXC11 and SPHK1 are highly expressed in HNSCC and might be involved in the Wnt signaling pathway. HOXC11 promoted cell proliferation, migration, and invasion, inhibiting apoptosis in HNSCC. Silencing SPHK1 inhibited cell progression and dysregulated the Wnt signaling pathway in HNSCC. Overexpressed SPHK1 reversed the functions of sh-HOXC11 in regulating cell progression and the Wnt signaling pathway. HOXC11 promotes HNSCC progression by regulating SPHK1 through the Wnt signaling pathway. Silencing HOXC11 inhibited the tumor growth of HNSCC. Our study demonstrates that HOXC11 promotes HNSCC progression by regulating SPHK1 through the Wnt/β-catenin signaling pathway, identifying a previously unrecognized regulatory axis in HNSCC.</p><p></p>

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

  • 期刊论文

  • 发表日期：

    2026年7月25日

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  • Jing Zhang,
  • Qionghui Wu,
  • Jingyuan Liu,
  • Shisheng Li

摘要

The discovery of potential targets in Head and neck squamous cell carcinomas (HNSCC) through molecular and mechanism analyses is crucial for understanding and treating this disease. This study utilized rigorous methods, including cell lines (FaDu and SCC-15) and a xenograft tumor model. Transfections were conducted using the Lipofectamine 2000 kit, and the evaluation of HOXC11, SPHK1, apoptosis-related protein, and the Wnt signaling pathway was carried out using qPCR and WB methods. The cell proliferation, migration, invasion, and apoptosis were comprehensively evaluated using colony formation, Transwell, wound healing, and flow cytometry, respectively. HOXC11 and SPHK1 are highly expressed in HNSCC and might be involved in the Wnt signaling pathway. HOXC11 promoted cell proliferation, migration, and invasion, inhibiting apoptosis in HNSCC. Silencing SPHK1 inhibited cell progression and dysregulated the Wnt signaling pathway in HNSCC. Overexpressed SPHK1 reversed the functions of sh-HOXC11 in regulating cell progression and the Wnt signaling pathway. HOXC11 promotes HNSCC progression by regulating SPHK1 through the Wnt signaling pathway. Silencing HOXC11 inhibited the tumor growth of HNSCC. Our study demonstrates that HOXC11 promotes HNSCC progression by regulating SPHK1 through the Wnt/β-catenin signaling pathway, identifying a previously unrecognized regulatory axis in HNSCC.