Visfatin is a pro-inflammatory cytokine, which is thought to play a central role in systemic inflammation and the pathogenesis of obesity related diseases. Only a few studies investigated the effect of visfatin on human cancers. Furthermore, there have been no studies on the association between the expression of visfatin in OSCC tissue and its effect on OSCC patients. Hence, the present study analyzed the expression of visfatin in OSCC from Korean patients. Immunohistochemistry for visfatin was performed using 12 normal oral mucosas (NOM), 16 oral leukoplakias (with/without dysplasia), and 58 OSCC patients samples. Immunoreactivity was semi-quantitatively scored and the correlation between the expression of visfatin and clinicopathological parameters of OSCC patients was analyzed. The immunohistochemical analysis demonstrated that the expression level of visfatin increased in OSCC alone (p<0.05). Moreover, the immunoexpression score of visfatin was significantly correlated with TNM stage of OSCC patients. Our findings suggested that visfatin can play a certain role in the pathogenesis of OSCC. In addition, visfatin was associated with the tumor progression of OSCC patients and may act as independent biomarker of OSCC.

Eukaryotic translation initiation factor 5A (eIF-5A) is essential for proliferation of eukaryotic cells, andwas identified as diagnotic marker in cervical intraepithelial neoplasia, cervical and endometrial cancer, but relatively little is known about thein vivo and in vitro expression patterns of eIF-5A in oral premalignant and malignant lesions mirror the expression levels observed in vitro with cells derived from normal oral mucosa, immortalized oral keratinocytes (IHOK) and primary and metastatic oral squamous cell carcinoma (OSCC). We used an oral squamous cell carcinoma (OSCC) progression model composed of cell lines and tissue specimens to characterize expression patterns by Western blotting and immunohistochemistry. eIF-5A and PCNA levels are elevated in IHOKand primary and metastatic OSCC cella as compatred to normal human oral keraitinocytes. eIF5A and PCNA expression was l imited to basal cells of normal oral mucosa. eIF-5A and PCNA expression is increased in dysplastic epithelium spreading to more superficial layers, and its expression levels correlated significantly with the degree of dysplasia. Well and moderately differentiated OSCC showed strong expression of eIF-5A and PCNA. These results suggest that upregulated expression of eIF-5A seems to be an important epigenetic alteration that accompanies oral carcinogenic progression, and eIF-5A could be used as an biomarker for oral premalignat lesion or squamous cell carcinoma