Bone Cancer Research Today is a free monthly online journal that collates and summarizes the latest research about Bone Cancer, including details on symptoms, types, treatment. | ||||||||
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Ganglioside GD1a suppresses TNFalpha expression via Pkn1 at the transcriptional level in mouse osteosarcoma-derived FBJ cells.Wang L, Wang Y, Sato T, Yamagata S, Yamagata T Laboratory of Tumor Biology and Glycobiology, Department of Life Sciences and Biopharmaceutics, Shenyang Pharmaceutical University, PO Box 29, 103 WenHua Road, Shenyang, LiaoNing 110016, People's Republic of China. Ganglioside GD1a has been reported to suppress metastasis [S. Hyuga, S. Yamagata, Y. Takatsu, M. Hyuga, H. Nakanishi, K. Furukawa, T. Yamagata, Suppression of FBJ-LL cell adhesion to vitronectin by ganglioside GD1a and loss of metastatic capacity, International J. Cancer. 83 (1999) 685-691.] and MMP-9 production in mouse osteosarcoma FBJ cells [D. Hu, Z. Man, P. Wang, X. Tan, X. Wang, S. Takaku, S. Hyuga, T. Sato, X. Yao, S. Yamagata, T. Yamagata, Ganglioside GD1a negatively regulates MMP9 expression in mouse FBJ cell lines at the transcriptional level, Connect. Tissue Res. 48 (2007) 198-205.]. In the present study, TNFalpha increased cell motility and MMP-9 and TNFalpha expression at the transcriptional level. TNFalpha expression was found to be inversely proportional to GD1a content in the FBJ-cell variants. The addition of exogenous GD1a to FBJ-LL cells suppressed TNFalpha expression, and treatment of FBJ-S1 cells with D-PDMP (glucosylceramide synthesis inhibitor) led to an increase in TNFalpha, indicating that TNFalpha is negatively regulated by GD1a in FBJ cells. SiRNA of Pkn1, a Rho-GTPase effecter protein kinase, suppressed TNFalpha levels as well as Pkn1 expression, suggesting that Pkn1 is involved in TNFalpha signaling. Treatment of Pkn1-silenced FBJ-LL cells with GD1a failed to suppress TNFalpha expression, demonstrating that GD1a signals that lead to TNFalpha suppression are transduced through Pkn1. Published 16 May 2008 in Biochem Biophys Res Commun, 371(2): 230-5.
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