ucn-1028-c and Nasopharyngeal-Neoplasms

Basic fibroblast growth factor (bFGF) is a strong mitogenic factor and inducer of angiogenesis. It may play an important role in the growth of solid tumors. Whereas bFGF is known to act extracellularly, the protein lacks a transient signal peptide. No defined mechanism for bFGF secretion has been characterized besides release from dead or injured cells. To explore molecular mechanism that modulates bFGF release, we treated CNE-2 cells with PMA for two days and found that the treatment increased bFGF gene expression in the cytoplasm and bFGF release significantly after 48 hours. This result suggests that protein kinase C is very likely to be involved in the bFGF release regulation. Our results have also shown that PKC-alpha activated by PMA in CNE-2 cells can phosphorylate bFGF (18 KDa) in CNE-2 cells. The result suggests that PKC-alpha translocation and activation can phosphorylate bFGF in CNE-2 cells and increase bFGF release.

Topics: Enzyme Inhibitors; Fibroblast Growth Factor 2; Humans; Naphthalenes; Nasopharyngeal Neoplasms; Protein Kinase C; Tetradecanoylphorbol Acetate; Tumor Cells, Cultured