BACKGROUND: Epithelial-mesenchymal transition (EMT) is a crucial process in 
cancer progression that provides cancer cells with the ability to escape from 
the primary focus, invade stromal tissues and migrate to distant regions. Cell 
lines that lack E-cadherin show increased tumorigenesis and metastasis, and the 
expression levels of E-cadherin and Snail correlate inversely with the prognosis 
of patients suffering from breast cancer or oral squamous cell carcinoma (OSCC). 
Moreover, recent studies have shown that most EMT cases are regulated by soluble 
growth factors or cytokines. Among these factors, fibroblast growth factors 
(FGFs) execute diverse functions by binding to and activating members of the FGF 
receptor (FGFR) family, including FGFR1-4. Fibroblast growth factor receptor 1 
is an oncoprotein that is involved in tumorigenesis, and PD173074 is known to be 
a selective inhibitor of FGFR1. However, the roles of FGFR1 and FGFR1 inhibitors 
have not yet been examined in detail.
METHODS: Here, we investigated the expression of FGFR1 in head and neck squamous 
cell carcinoma (HNSCC) and the role of the FGFR1 inhibitor PD173074 in 
carcinogenesis and the EMT process.
RESULTS: Fibroblast growth factor receptor 1 was highly expressed in 54% of 
HNSCC cases and was significantly correlated with malignant behaviours. Nuclear 
FGFR1 expression was also observed and correlated well with histological 
differentiation, the pattern of invasion and abundant nuclear polymorphism. 
Fibroblast growth factor receptor 1 was also overexpressed in EMT cell lines 
compared with non-EMT cell lines. Furthermore, treatment of HOC313 cells with 
PD173074 suppressed cellular proliferation and invasion and reduced ERK1/2 and 
p38 activation. These cells also demonstrated morphological changes, 
transforming from spindle- to cobble stone-like in shape. In addition, the 
expression levels of certain matrix metalloproteinases (MMPs), whose genes 
contain activator protein-1 (AP-1) promoter sites, as well as Snail1 and Snail2 
were reduced following PD173074 treatment.
CONCLUSION: Taken together, these data suggest that PD173074 inhibits the MAPK 
pathway, which regulates the activity of AP-1 and induces MET. Furthermore, this 
induction of MET likely suppresses cancer cell growth and invasion.