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Updated: Aug 4, 2025
A Model for Perineural Invasion in Head and Neck Squamous Cell Carcinoma
Published on: January 5, 2017
SEC11A contributes to tumour progression of head and neck squamous cell carcinoma
Hailong Shen1, Fangzheng Yi1, Zhao Ding1
1Department of Otolaryngology-Head & Neck Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, PR China.
Background:
Head and neck squamous cell carcinoma (HNSCC) is a prevalent disease that has a low survival rate and high recurrence risk. Our study aims to investigate the expression and role of SEC11A in HNSCC.
Methods:
The expression of SEC11A was assessed in 18 pairs of cancerous and adjacent tissues by qRT-PCR and western blotting. Immunohistochemistry was performed in clinical specimen sections to evaluate the expression of SEC11A and its association with outcomes. Furthermore, the functional role of SEC11A in HNSCC tumor proliferation and progression was investigated using the in vitro cell model with lentivirus-mediated SEC11A knockdown. Colony formation and CCK8 assays were conducted to assess cell proliferation potential, while in vitro migration and invasion were examined using wound healing and transwell assays. To determine the tumor formation potential in vivo, a tumor xenograft assay was used.
Results:
In contrast to adjacent normal tissues, SEC11A expression was significantly elevated in HNSCC tissues. SEC11A was mainly localized in the cytoplasm, and its expression was significantly associated with patient prognosis. SEC11A was silenced using shRNA lentivirus in TU212 and TU686 cell lines, and the gene knockdown was confirmed. A series of functional assays demonstrated that SEC11A knockdown reduced cell proliferation, migration and invasion ability in vitro. In addition, the xenograft assay demonstrated that SEC11A knockdown significantly inhibited tumor growth in vivo. Tumor tissue sections of mice showed decreased proliferation potential in the shSEC11A xenografts cells by immunohistochemistry.
Conclusion:
SEC11A knockdown decreased cell proliferation, migration and invasion in vitro and subcutaneous tumorigenesis in vivo. SEC11A is crucial to HNSCC proliferation and progression, and may serve as a new therapeutic target.
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