Open AccessSprouty2 protein is downregulated in human squamous cell carcinoma of the head and neck and suppresses cell proliferation in vitro
Author(s) -
Chiang Liang Lin,
Wei Fan Chiang,
Chao Ling Tung,
Jeng Long Hsieh,
Jenn Ren Hsiao,
Wen-Cheng Huang,
Feng Li,
Chi Hua Chang,
Shyun Yeu Liu,
Chao Jung Tsao,
Feng Yin
Publication year - 2014
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2014.2700
Subject(s) - head and neck squamous cell carcinoma , cancer research , carcinogenesis , cell growth , protein kinase b , cell cycle , oncogene , pi3k/akt/mtor pathway , biology , medicine , pathology , signal transduction , cancer , head and neck cancer , microbiology and biotechnology , genetics
Sprouty2 is known for its tumor-suppressing effect in various human malignant diseases. In head and neck squamous cell carcinoma (HNSCC), the role of sprouty2 in tumorigenesis and clinical implication remains elusive. The aim of the present study was to investigate the expression of sprouty2 in patients with HNSCC and its function in vitro. Quantitative analysis of mRNA expression of sprouty2 was performed on frozen tumor samples from 42 patients with HNSCC and 19 with oral verrucous hyperplasia (OVH) with paired counterparts of normal mucosa. Downregulation of sprouty2 expression was demonstrated in 79% of HNSCC samples and in 58% of OVH samples compared with paired samples of normal mucosa. Enhanced expression of sprouty2 protein suppressed the growth of HNSCC cells and signaling of the phosphorylated AKT pathway. Following transfection of the sprouty2 plasmid, HNSCC cells were more sensitive to sorafenib, a tyrosine kinase inhibitor of Raf and vascular endothelial growth factor receptor. The present study suggested that sprouty2 expression was downregulated and behaved as a tumor suppressor in HNSCC. Sprouty2 expression in tumor cells enhanced sensitivity to sorafenib. Further studies are required to define the clinical impact of sprouty2 in patients with HNSCC.