Oncotarget

Research Papers:

STC2 promotes head and neck squamous cell carcinoma metastasis through modulating the PI3K/AKT/Snail signaling

Shuwen Yang _, Qinghai Ji, Bin Chang, Yan Wang, Yongxue Zhu, Duanshu Li, Caiping Huang, Yulong Wang, Guohua Sun, Ling Zhang, Qing Guan, Jun Xiang, Wenjun Wei, Zhongwu Lu, Tian Liao, Jiao Meng, Ziliang Wang, Ben Ma, Li Zhou, Yu Wang and Gong Yang

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Oncotarget. 2017; 8:5976-5991. https://doi.org/10.18632/oncotarget.13355

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Abstract

Shuwen Yang1,2,3,*, Qinghai Ji1,2,3,*, Bin Chang2,4, Yan Wang2,3, Yongxue Zhu1,2, Duanshu Li1,2, Caiping Huang1,2, Yulong Wang1,2, Guohua Sun1,2, Ling Zhang1,2, Qing Guan1,2, Jun Xiang1,2, Wenjun Wei1,2, Zhongwu Lu1,2, Tian Liao1,3, Jiao Meng3, Ziliang Wang3, Ben Ma1,2,3, Li Zhou1,2,3, Yu Wang1,2,3, Gong Yang2,3,5

1Department of Head & Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China

2Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China

3Cancer Research Institute, Fudan University Shanghai Cancer Center, Shanghai 200032, China

4Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China

5Central Laboratory, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai 200240, China

*Co-First authors

Correspondence to:

Yu Wang, email: neck130@hotmail.com

Gong Yang, email: yanggong@fudan.edu.cn

Keywords: STC2, pAKT, Snail, HNSCC, metastasis

Received: May 23, 2016    Accepted: October 14, 2016    Published: November 15, 2016

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.


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