Research Papers:

Peroxiredoxin 1 promotes invasion and migration by regulating epithelial-to-mesenchymal transition during oral carcinogenesis

Wenwen Niu, Min Zhang, Hui Chen, Chunxiao Wang, Ni Shi, Xinying Jing, Lihua Ge, Tong Chen and Xiaofei Tang _

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Oncotarget. 2016; 7:47042-47051. https://doi.org/10.18632/oncotarget.9705

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Wenwen Niu1,*, Min Zhang1,*, Hui Chen1, Chunxiao Wang1, Ni Shi2, Xinying Jing1, Lihua Ge1, Tong Chen2,#, Xiaofei Tang1,#

1Division of Oral Pathology, Beijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Dongcheng District, Beijing, China

2Division of Medical Oncology, Department of Internal Medicine, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Columbus, Ohio, USA

*These authors contributed equally to this work

#These authors shared senior authorship

Correspondence to:

Xiaofei Tang, email: [email protected]

Tong Chen, email: [email protected]

Keywords: peroxiredoxin 1, NFκB, oral squamous cell carcinoma, epithelial-to-mesenchymal transition, nicotine

Received: September 02, 2015     Accepted: May 20, 2016     Published: May 30, 2016


Tobacco smoking is the major risk factor for oral squamous cell carcinoma (OSCC). Previously, we found that nicotine up-regulates peroxiredoxin 1 (Prx1), an important antioxidant enzyme, and nuclear factor kappa B (NFκB) in OSCC cells. However, the molecular mechanism of Prx1 in oral carcinogenesis remains obscure. To improve our understanding of the functional role of Prx1 during the cascade of tobacco-associated oral carcinogenesis, we characterized Prx1, NFκB, and epithelial-to-mesenchymal transition (EMT) markers including E-cadherin, vimentin and Snail in 30 primary oral tumors (15 from smokers with OSCC and 15 from non-smokers with OSCC) and 10 normal oral mucosa specimens from healthy individuals. The expression levels of Prx1, nuclear NFκB, vimentin and Snail were higher in the tumors from smokers with OSCC than in those from non-smokers with OSCC or the healthy controls. The expression levels of E-cadherin showed an opposite trend. Prx1 silencing suppressed the nicotine-induced EMT, cell invasion and migration in SCC15 cells in vitro. Furthermore, Prx1 activated the NFκB pathway in SCC15 cells. Prx1 might therefore play an oncogenic role in tobacco-related OSCC and thus serve as a target for chemopreventive and therapeutic interventions.

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