Koichiro Kato1, Miyako Shimasaki2, Takao Kato3, Natsuki Segami3, Yoshimichi Ueda2. 1. Department of Oral and Maxillofacial Surgery, Kanazawa Medical University, Ishikawa, Japan k-kato@kanazawa-med.ac.jp. 2. Department of Pathophysiological and Experimental Pathology, Kanazawa Medical University, Ishikawa, Japan. 3. Department of Oral and Maxillofacial Surgery, Kanazawa Medical University, Ishikawa, Japan.
Abstract
BACKGROUND/AIM: The expression of sphingosine kinase-1 (SphK1) has been reported in several cancers. However, the exact roles of SphK1 in cancer progression still remain unknown. The aim of the present study was to investigate SphK1 expression in oral squamous cell carcinoma (OSCC) and clarify the involvement of SphK1 in the proliferation and invasiveness of OSCC and its prognostic implications. MATERIALS AND METHODS: Expression of SphK1, E-cadherin, vimentin, and Ki-67 were examined in 69 OSCC tissues immunohistochemically, as well as by western blot, and correlations between their expression and relationships with tumor invasiveness and prognosis were analyzed. RESULTS: SphK1 was expressed in the tumor cells of 38 of 69 OSCCs, particularly at the invasion front. Patients with OSCCs with high SphK1 expression showed higher invasive grades and unfavorable survival rates. SphK1 expression correlated with acquisition of vimentin expression and loss of E-cadherin expression; there was no significant difference in Ki-67 labeling indices between OSCCs with high and low SphK1 expression. CONCLUSION: These results demonstrate the involvement of SphK1 in the invasiveness of OSCC and in unfavorable prognosis, indicating its role in the epithelial-mesenchymal transition of OSCC cells. Copyright
BACKGROUND/AIM: The expression of sphingosine kinase-1 (SphK1) has been reported in several cancers. However, the exact roles of SphK1 in cancer progression still remain unknown. The aim of the present study was to investigate SphK1 expression in oral squamous cell carcinoma (OSCC) and clarify the involvement of SphK1 in the proliferation and invasiveness of OSCC and its prognostic implications. MATERIALS AND METHODS: Expression of SphK1, E-cadherin, vimentin, and Ki-67 were examined in 69 OSCC tissues immunohistochemically, as well as by western blot, and correlations between their expression and relationships with tumor invasiveness and prognosis were analyzed. RESULTS:SphK1 was expressed in the tumor cells of 38 of 69 OSCCs, particularly at the invasion front. Patients with OSCCs with high SphK1 expression showed higher invasive grades and unfavorable survival rates. SphK1 expression correlated with acquisition of vimentin expression and loss of E-cadherin expression; there was no significant difference in Ki-67 labeling indices between OSCCs with high and low SphK1 expression. CONCLUSION: These results demonstrate the involvement of SphK1 in the invasiveness of OSCC and in unfavorable prognosis, indicating its role in the epithelial-mesenchymal transition of OSCC cells. Copyright