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Updated: Jan 22, 2026

A Model for Perineural Invasion in Head and Neck Squamous Cell Carcinoma
Published on: January 5, 2017
Long non-coding RNA HOTAIR/microRNA-206 sponge regulates STC2 and further influences cell biological functions in
Tiancheng Li1, Yao Qin1, Zhen Zhen1
1Department of Otorhinolaryngology-Head and Neck Surgery, Peking University First Hospital, Beijing, China.
Objective:
It is essential to characterize underlying molecular mechanism associated with head and neck squamous cell carcinoma (HNSCC) and identify promising therapeutic targets. Herein, we explored role of homeobox transcript antisense RNA (HOTAIR) in HNSCC to regulate stanniocalcin-2 (STC2) by sponging microRNA-206 (miR-206).
Methods:
HNSCC-related differentially expressed genes and regulation network amongst HOTAIR, miR-206 and STC2 were identified. Next, effect of HOTAIR on cell biological functions of HNSCC was identified after transfection of cells with HOTAIR overexpressed plasmids or siRNA against HOTAIR. PI3K/AKT signalling pathway-related gene expression was measured after miR-206 and STC2 were suppressed. Cell invasion, migration and proliferation were assessed. Finally, tumour growth was assessed to determine the effects of HOTAIR/miR-206/STC2 axis in vivo.
Results:
HOTAIR specifically bound to miR-206 and miR-206 targeted STC2. Downregulated HOTAIR or upregulated miR-206 suppressed HNSCC cell proliferation, invasion and migration. miR-206 inhibited PI3K/AKT signalling pathway by down-regulating STC2. Besides, silenced HOTAIR or overexpressed miR-206 repressed the tumour growth of nude mice with HNSCC.
Conclusion:
HOTAIR regulated HNSCC cell biological functions by binding to miR-206 through STC2.
Insights
Homeobox transcript antisense RNA (HOTAIR) promotes head and neck squamous cell carcinoma (HNSCC) progression by sponging microRNA-206 (miR-206) to upregulate stanniocalcin-2 (STC2). Inhibiting HOTAIR or boosting miR-206 hinders HNSCC growth.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Head and neck squamous cell carcinoma (HNSCC) is a prevalent cancer requiring novel therapeutic targets.
- Understanding the molecular mechanisms driving HNSCC is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the role of homeobox transcript antisense RNA (HOTAIR) in HNSCC.
- To elucidate the regulatory axis involving HOTAIR, microRNA-206 (miR-206), and stanniocalcin-2 (STC2) in HNSCC.
- To identify potential therapeutic targets for HNSCC treatment.
Main Methods:
- Differential gene expression analysis and network construction to identify the HOTAIR/miR-206/STC2 regulatory network.
- In vitro experiments involving HOTAIR overexpression and knockdown to assess effects on HNSCC cell functions (proliferation, invasion, migration).
- In vivo tumor growth assays in nude mice to evaluate the therapeutic potential of targeting the HOTAIR/miR-206/STC2 axis.
Main Results:
- HOTAIR was found to directly bind to miR-206, which in turn targets STC2.
- Downregulation of HOTAIR or upregulation of miR-206 significantly inhibited HNSCC cell proliferation, invasion, and migration.
- miR-206 suppressed the PI3K/AKT signaling pathway by downregulating STC2.
- Silencing HOTAIR or overexpressing miR-206 repressed HNSCC tumor growth in vivo.
Conclusions:
- HOTAIR plays a critical role in regulating HNSCC cell biological functions.
- The HOTAIR/miR-206/STC2 axis represents a significant molecular pathway in HNSCC.
- Targeting this axis holds promise for HNSCC therapeutic strategies.
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