IADR Abstract Archives
Immunohistochemical study on the expression of PRL-3 in human oral squamous cell carcinoma and rat carcinogensis model
Objectives: PRL is a member of small class of tyrosine phosphatases consisting of three members (PRL-1, PRL-2 and PRL-3), sharing a high degree (>75%) of amino acid sequence identity. Several lines of evidence have shown that PRL-3 is associated with the progression of colon tumor including gastric tumors, melanomas, prostate tumors, pancreatic tumors, ovarian tumors and Hodgkins lymphoma. However, the correlation between PRL-3 expression and clinical outcome in oral squamous cell carcinoma (OSCC) has not been studied yet. Here we assessed roles of PRL-3 in tumorigenesis, progression of human OSCC and rat carcinogenesis model.
Methods: We analyzed PRL-3, p53, Ki-67, Bax, Bcl-2, Ck10/13, Ck-17, CK-19 expression by immunohistochemistry in 91 human oral SCC, 32 dysplasia and 20 normal mucosa tissues. We then compared the clinicopathological characteristics of the PRL-3 positive and negative carcinoma and the overall survival rate was compared between the patients with high PRL-3 expression (n =56) and those with moderate or low PRL-3 expression (n = 35) in OSCC. Male wistar rats are distributed in three group of 10 animal each and treated with 40 ppm 4NQO solutions though drinking water for 4, 12 and 20 weeks. Ten animals were used as negative control. PCNA and PRL-3 expressions were analyzed by Immunohistochemistry.
Results: In immunohistochemistry, PRL-3 expressions were significantly higher in SCC and dysplasia than in normal mucosa (p = 0.0310, p < 0.0001, respectively,). PRL-3 expression were correlated with histological differentiation (p = 0.0001), and not positively correlated with patients' clinical stages and LN metastasis and overall survival rate. High expression of PRL-3 is significantly correlated with epithelial differentiation marker CK-17 (p = 0.0006). In addition, PRL-3 has shown high expression in dysplasia, cancer tissues than the normal epithelium of rat tongue.
Conclusions: Our results suggest that PRL-3 plays a key role in tumorigenesis and it may be a novel marker of oral cancer progression.
Methods: We analyzed PRL-3, p53, Ki-67, Bax, Bcl-2, Ck10/13, Ck-17, CK-19 expression by immunohistochemistry in 91 human oral SCC, 32 dysplasia and 20 normal mucosa tissues. We then compared the clinicopathological characteristics of the PRL-3 positive and negative carcinoma and the overall survival rate was compared between the patients with high PRL-3 expression (n =56) and those with moderate or low PRL-3 expression (n = 35) in OSCC. Male wistar rats are distributed in three group of 10 animal each and treated with 40 ppm 4NQO solutions though drinking water for 4, 12 and 20 weeks. Ten animals were used as negative control. PCNA and PRL-3 expressions were analyzed by Immunohistochemistry.
Results: In immunohistochemistry, PRL-3 expressions were significantly higher in SCC and dysplasia than in normal mucosa (p = 0.0310, p < 0.0001, respectively,). PRL-3 expression were correlated with histological differentiation (p = 0.0001), and not positively correlated with patients' clinical stages and LN metastasis and overall survival rate. High expression of PRL-3 is significantly correlated with epithelial differentiation marker CK-17 (p = 0.0006). In addition, PRL-3 has shown high expression in dysplasia, cancer tissues than the normal epithelium of rat tongue.
Conclusions: Our results suggest that PRL-3 plays a key role in tumorigenesis and it may be a novel marker of oral cancer progression.