Knockdown of Stanniocalcin-1 inhibits growth and glycolysis in oral squamous cell carcinoma cells

被引:1
|
作者
Wang, Chanyuan [2 ,3 ]
Hu, Jianpei [1 ]
Wang, Lijian [3 ]
机构
[1] Lishui Peoples Hosp, Dept Stomatol, 15 Dazhong St, Lishui 323000, Zhejiang, Peoples R China
[2] Zhejiang Univ Chinese Med, Grad Sch, Hangzhou 310053, Zhejiang, Peoples R China
[3] Lishui Peoples Hosp, Dept Stomatol, Lishui 323000, Zhejiang, Peoples R China
来源
OPEN LIFE SCIENCES | 2024年 / 19卷 / 01期
关键词
oral squamous cell carcinoma; Stanniocalcin-1; growth; glycolysis; PI3K/Akt pathway;
D O I
10.1515/biol-2022-0907
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Oral squamous cell carcinoma (OSCC) is the most common malignancy among head and neck squamous cell carcinomas. Targeted therapy plays a crucial role in the treatment of OSCC. However, new and more targets are still needed to develop. Stanniocalcin-1 (STC-1) is a glycoprotein hormone that affects the progression of cancers. However, the potential role of STC-1 in OSCC progression remains to be explored. Here, we aimed to elucidate the role of STC-1 in OSCC. We revealed that STC-1 was highly expressed in OSCC tissues and is correlated with poor patient prognosis. Knockdown of STC-1 significantly suppressed the growth of OSCC cells and restrained glycolysis by reducing glucose consumption, ATP production, and lactate levels. Mechanistically, STC-1 ablation inhibited the PI3K/Akt pathway, reducing the phosphorylation levels of PI3K and Akt. In conclusion, STC-1 depletion restrained OSCC cell growth and glycolysis via PI3K/Akt pathway and has the potential to serve as a therapeutic target for OSCC.
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页数:8
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