,Inhibition of fibroblast growth factor 2-induced apoptosis involves survivin expression, protein ki

• 作 者: Desheng Xiao Kuansong Wang Jianhua Zhou Huiqiu Cao Zhenghao Deng Yongbin Hu Xiahui Qu Jifang Wen
• 机 构: Department of Pathology, Xiangya School of Medicine, Central South University, Chang sha 410013, Chi
• 出 处: 生物化学与生物物理学报（英文版）
• 发表日期: 2008年4期
• 关键词: FGF-2 survivin Smac PKC apoptosis lung cancer

To investigate the mechanism by which fibroblast growth factor 2 (FGF-2) inhibits apoptosis in the human small cell lung cancer cell line H446 subjected to serum starvation,apoptosis was evaluated by flow cytometry, Hoechst 33258 staining, caspase-3 activity, and DNA fragmentation.Survivin expression induced by FGF-2 and protein kinase Cα (PKCα) translocation was detected by subcellular fractionation and Weste blot analysis. In addition, FGF-2-induced release of Smac from mitochondria to the cytoplasm was analyzed by Weste blotting and immunofluorescence.FGF-2 reduced apoptosis induced by serum starvation and up-regulated survivin expression in H446 cells in a dosedependent and time-dependent manner, and inhibited caspase-3 activity. FGF-2 also inhibited the release of Smac from mitochondria to the cytoplasm induced by serum starvation and increased PKCα translocation from the cytoplasm to the cell membrane. In addition, PKC inhibitor inhibited the expression of survivin. FGF-2 up-regulates the expression of survivin protein in H446 cells and blocks the release of Smac from mitochondria to the cytoplasm. PKCα regulated FGF-2-induced survivin expression. Thus, survivin, Smac,and PKCα might play important roles in the inhibition of apoptosis by FGF-2 in human small cell lung cancer cells.