BACKGROUND: Salivary gland tumors (SGT) are rare lesions with uncertain histopathology. One of the major signaling pathways that participate in the development of several tumors is protein kinase A. In this pathway, glycogen synthase kinase β (GSK3β) and cAMP responsive element binding protein (CREB3) are two genes which are supposed to be down regulated in most human tumors. The expression level of the genes was evaluated in SGT to scrutinize their possible under expression in these tumors. METHODS: Forty eight fresh tissue samples were obtained from patients with benign and malignant SGT, including pleomorphic adenoma, warthin's tumor, mucoepidermoid carcinoma (MEC), salivary duct carcinoma and carcinoma ex pleomorphic adenoma. Eight normal samples were used as controls. Quantitative real-time PCR was used to analyze the expression level of interest genes. RESULTS: Data was analyzed by statistical methods. GSK3β was downregulate in all samples and all results were statistically significant (P<0.05). CREB3 did not show a significant decrease or increase in its mRNA expression, but the results were significant in MEC and salivary duct carcinoma. CONCLUSION: GSK3β down regulation has been reported in many human tumors. This gene stimulates CREB3, inducing cell proliferation and oncogenesis. Our findings showed GSK β down regulation; however, CREB3 expression level was close to normal group. No association between CREB3 expression and inactivated GSK3β could be postulated in SGT.
BACKGROUND:Salivary gland tumors (SGT) are rare lesions with uncertain histopathology. One of the major signaling pathways that participate in the development of several tumors is protein kinase A. In this pathway, glycogen synthase kinase β (GSK3β) and cAMP responsive element binding protein (CREB3) are two genes which are supposed to be down regulated in most humantumors. The expression level of the genes was evaluated in SGT to scrutinize their possible under expression in these tumors. METHODS: Forty eight fresh tissue samples were obtained from patients with benign and malignant SGT, including pleomorphic adenoma, warthin's tumor, mucoepidermoid carcinoma (MEC), salivary duct carcinoma and carcinoma ex pleomorphic adenoma. Eight normal samples were used as controls. Quantitative real-time PCR was used to analyze the expression level of interest genes. RESULTS: Data was analyzed by statistical methods. GSK3β was downregulate in all samples and all results were statistically significant (P<0.05). CREB3 did not show a significant decrease or increase in its mRNA expression, but the results were significant in MEC and salivary duct carcinoma. CONCLUSION: GSK3β down regulation has been reported in many humantumors. This gene stimulates CREB3, inducing cell proliferation and oncogenesis. Our findings showed GSK β down regulation; however, CREB3 expression level was close to normal group. No association between CREB3 expression and inactivated GSK3β could be postulated in SGT.
Authors: Keiko Miyoshi; Andrea Rosner; Masahiro Nozawa; Christopher Byrd; Fanta Morgan; Esther Landesman-Bollag; Xin Xu; David C Seldin; Emmett V Schmidt; Makato M Taketo; Gertraud W Robinson; Robert D Cardiff; Lothar Hennighausen Journal: Oncogene Date: 2002-08-15 Impact factor: 9.867
Authors: Shin-Ichiro Maruya; Hyung-Woo Kim; Randal S Weber; Jack J Lee; Merril Kies; Mario A Luna; John G Batsakis; Adel K El-Naggar Journal: J Mol Diagn Date: 2004-08 Impact factor: 5.568