Abstract
Objectives
Rap1 has been shown to be activated in response to various growth factors, cytokines, and chemokines that act on receptor tyrosine kinases (RTKs) or G-protein-coupled receptors, and implicated in a wide range of biochemical pathways in all eukaryotic cells through a number of distinct effectors. This study was aimed to investigate the role of RAP1 in the tumorigenesis of squamous cell carcinoma of head and neck (HNSCC).
Methods
Immunohistochemical analysis was performed to study RAP1, CK 10, and E-cadherin expressions on the paraffin-embedded tissue of 198 HNSCCs. The relationship between RAP1 expression and the clinical prognosis was also investigated.
Results
RAP1 expression was readily detected in the normal epithelium and the well-differentiated HNSCC, whereas its expression turned to be weak or undetectable in the poorly differentiated HNSCC (p < 0.001). When RAP1 expression was decreased, the expressions of CK 10 (differentiation marker) and E-cadherin protein were also down regulated. In addition, patients with high RAP1 expression had significantly longer median survival than patients with low RAP1 expression (median = 51.21 vs. 13.14 months, p <0.001) by survival analysis based on the Kaplan-Meier method.
Conclusions
RAP1 expression may be related to cell differentiation in HNSCC. In addition, RAP1 could be a useful biomarker for tumor progression and survival of HNSCC.
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