Expression of podoplanin and E-cadherin in oral squamous cell carcinoma and oral epithelial dysplasia

• Main Authors: Chia-Jung Lin, 林佳蓉
• Other Authors: CHUN-PIN CHIANG
• Format: Others
• Language: en_US
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/28383620043852821626

碩士 === 國立臺灣大學 === 臨床牙醫學研究所 === 97 === Background and purposes: The transformation from stable epithelial cell to the mesenchymal phenotype, named as epithelial-mesenchymal transition (EMT), was noted in the process of carcinoma invasion. The podoplanin, a specific lymphatic marker, is involved in the process of the cancer invasion in a variety of human carcinomas. In this study, we investigated the expression of podoplanin and E-cadherin in the normal oral mucosa (NOM), oral epithelial dysplasia (OED), and oral squamous cell carcinoma (OSCC) samples to understand their association with tumor invasion, clinicopathological parameters, and patients’ survival. Materials and methods: The expression of podoplanin and E-cadherin in NOM, OED, and OSCC samples was evaluated by immunohistochemistry. The podoplanin and E-cadherin labeling scores (LSs) for NOM, OED, and OSCC samples and the intratumoral and peritumoral lymphatic vessel densities (iLVD and pLVD) in OSCC samples were counted and correlated with clinicopathological parameters and survival of OSCC patients. Results: We found that there was a significant reduction of the mean pLVD in OSCCs with larger tumor size (P = 0.000), with distant metastasis (P = 0.023), and with more advanced clinical stage (P = 0.001). In addition, there was also a significant decrease of the mean iLVD in OSCCs with larger tumor size (P = 0.010). OSCC patient with the pLVD < 34 vessels/100× field had a significantly poorer overall (P = 0.036) and disease-specific survival (P = 0.020) than those with the pLVD > 34 vessels/100× field. A significant increase in podoplanin expression was found in OSCCs with regional lymph node metastasis (P = 0.026), distant metastasis (P = 0.021), and less histologic differentiation (P = 0.013). Moreover, OSCC patient with the podoplanin LS > 20% had a significantly poorer overall survival than those with the podoplanin LS < 20% (P = 0.033). There was a significant decrease in E-cadherin expression in younger OSCC patients (P = 0.002) and in OSCCs with regional lymph node metastasis (P = 0.016) and less histologic differentiation (P = 0.001). OSCC patient with the E-cadherin LS < 150% had a significantly poorer overall (P = 0.016) and disease-specific survival (P = 0.005) than those with the E-cadherin LS > 150%. Furthermore, cancer cells in the invasion front with high podoplanin expression showed a significant loss of E-cadherin. Conclusions: The pLVD may act as a biomarker to predict the T status, clinical stage, and prognosis of OSCC patients. An increase of podoplanin expression and a loss of E-cadherin expression are noted during oral carcinogenesis and are associated with more lymph node metastasis and poorer prognosis of OSCC patients. This suggests that both podoplanin and E-cadherin LSs may be useful biomarkers for prediction of tumor metastasis in OSCCs and prognosis of OSCC patients. The podoplanin and E-cadherin may be involved in cancer invasion with EMT in most OSCCs. However, further studies on the mechanisms of OSCC invasion are needed.