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STC2 promotes head and neck squamous cell carcinoma metastasis through modulating the PI3K/AKT/Snail signaling
Shuwen Yang1,2,3, Qinghai Ji1,2,3, Bin Chang2,4
1Department of Head & Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China.
Abstract:
The mammalian peptide hormone stanniocalcin 2 (STC2) plays an oncogenic role in many human cancers. However, the exact function of STC2 in human head and neck squamous cell carcinoma (HNSCC) is unclear. We aimed to examine the function and clinical significance of STC2 in HNSCC. Using in vitro and in vivo assays, we show that overexpression of STC2 suppressed cell apoptosis, promoted cell proliferation, migration, invasion, and cell cycle arrest at the G1/S transition. By contrast, silencing of STC2 inhibited these activities. We further show that STC2 upregulated the phosphorylation of AKT and enhanced HNSCC metastasis via Snail-mediated increase of vimentin and decrease of E-cadherin. These responses were blocked by silencing of STC2/Snail expression or inhibition of pAKT activity. Furthermore, clinical data indicate that high STC2 expression was associated with high levels of pAKT and Snail in tumor samples from HNSCC patients with regional lymph node metastasis (P < 0.01). Thus, we conclude that STC2 controls HNSCC metastasis via the PI3K/AKT/Snail signaling axis and that targeted therapy against STC2 may be a novel strategy to effectively treat patients with metastatic HNSCC.
Insights
Stanniocalcin 2 (STC2) promotes head and neck cancer growth and metastasis by activating the AKT/Snail pathway. Targeting STC2 may offer a new treatment for metastatic head and neck squamous cell carcinoma (HNSCC).
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Stanniocalcin 2 (STC2) is implicated in various human cancers.
- The specific role of STC2 in head and neck squamous cell carcinoma (HNSCC) remains largely undefined.
Purpose of the Study:
- To investigate the function and clinical significance of STC2 in HNSCC.
- To elucidate the molecular mechanisms underlying STC2's role in HNSCC progression.
Main Methods:
- In vitro and in vivo assays were employed to assess STC2's effects on HNSCC cells.
- Western blotting and immunohistochemistry were used to analyze protein expression and phosphorylation.
- Clinical data from HNSCC patients were correlated with STC2 expression levels.
Main Results:
- STC2 overexpression promoted HNSCC proliferation, migration, invasion, and G1/S cell cycle arrest while suppressing apoptosis.
- STC2 upregulated AKT phosphorylation and enhanced metastasis through Snail-mediated modulation of vimentin and E-cadherin.
- High STC2 expression correlated with elevated pAKT and Snail levels in patients with lymph node metastasis.
Conclusions:
- STC2 drives HNSCC metastasis via the PI3K/AKT/Snail signaling pathway.
- STC2 represents a potential therapeutic target for treating metastatic HNSCC.
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