FA are structures of cell attachment to the extracellular matrix. Previously, we showed that bradykinin (BK) induces dissipation of vinculin-, but not talin-, staining FA by a mechanism that involves activation of PLC, suggesting that BK could be inducing

L.FIORE; C. LANG; MC. FERMENTO; NA GANDINI; HV MATURI; N.STERIN-SPEZIALE; AC CURINO; MM FACCHINETTI

Mar del Plata-Argentina

Congreso; 43 Reunión de la c; 2007

FA are structures of cell attachment to the extracellular matrix. Previously, we showed that bradykinin (BK) induces dissipation of vinculin-, but not talin-, staining FA by a mechanism that involves activation of PLC, suggesting that BK could be inducing

Sphingosine kinase-1 (SK1) is a key enzyme that regulates the balance between cellular levels of the pro-apoptotic molecules sphingosine (SPH) and ceramide (CER) and the growth-promoting lipid sphingosine-1-phosphate (S1P). SK1 has been shown to be upregulated in lung cancer and in glioblastoma and to confer resistance to chemotherapy in some cell types. However, few studies have been performed showing expression in human tumors. Therefore, we focused on studying the role that this protein plays in human tumor progression by analyzing its expression in breast and colon adenocarcinomas, gliomas, head and neck squamous cell carcinomas (HNSCC) and clear cell renal carcinomas (CCRC). We first performed a screening of SK1 expression in HNSCC samples by using the recently developed tissue array: we observed that the enzyme was expressed in 85.7% of tumors (162 out of 189). To obtain more qualitative information we studied different tumor tissues by regular immunohistochemistry and observed that the staining was stronger in tumor cells when compared with adjacent tissue and that it had a cytoplasmic localization. We also studied protein expression on a mouse model of breast cancer (MMTV-PyMT). The results shown confirmed that SK1 may play a role in human tumor progression.