Research Papers:
Differential expression of peroxiredoxin 3 in laryngeal squamous cell carcinoma
Metrics: PDF 1765 views | HTML 2132 views | ?
Abstract
Hua Zhang1,2,*, Xuexia Liu3,*, Lei Chen4,*, Li Cai5, Ning Li3, Peng Zhu3, Jian Chen3, Xicheng Song1, Guojun Li2,6
1Department of Otolaryngology-Head and Neck Surgery, Yuhuangding Hospital of Qingdao University, Yantai, China
2Department of Head and Neck Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
3Department of Central Laboratory, Yuhuangding Hospital of Qingdao University, Yantai, China
4Department of Clinical Laboratory, Yuhuangding Hospital of Qingdao University, Yantai, China
5Department of Pathology, Yuhuangding Hospital of Qingdao University, Yantai, China
6Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
*These authors have contributed equally to this work and are considered co-first authors
Correspondence to:
Xicheng Song, email: [email protected]
Guojun Li, email: [email protected]
Keywords: peroxiredoxin 3, laryngeal squamous cell carcinoma, Hep-2 cell line, oxidative stress
Received: November 10, 2016 Accepted: November 22, 2016 Published: December 09, 2016
ABSTRACT
Peroxiredoxin (PRDX) proteins are involved in carcinogenesis. PRDX3, which is predominantly localized in mitochondria and up-regulated in several human cancers, seems to confer increased treatment resistance and aggressive phenotypes. This study examined the expression profile of PRDX3 and its possible clinical value in laryngeal squamous cell carcinoma (LSCC). The expression of PRDX3 in LSCC samples was confirmed by Western blotting and further analyzed by immunohistochemistry in LSCC samples of different clinical pathological stages. The results showed that up-regulated expression of PRDX3 was observed in LSCC and associated with poor differentiation (P < 0.01), primary tumor location, N category and tumor stage (P < 0.05). Knockdown of PRDX3 in the Hep-2 laryngeal carcinoma epithelial cell line significantly enhanced Hep-2 cells’ apoptosis and inhibited their proliferation and migration. Taken together, our results suggest that PRDX3 has substantial clinical impact on the progression of LSCC and shed new light on the role of PRDX3 in treatment resistance and aggressive phenotypes in LSCC.
![Creative Commons License](/images/80x15.png)
PII: 13838