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Negative growth regulation of SK-N-MC cells by bFGF defines a growth factor-sensitive point in G_2

机译:BFGF的SK-N-MC细胞的负生长调节在G_2中定义了生长因子敏感点

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Basic fibroblast growth factor (bFGF) has been shown to induce growth inhibition and cell scattering of the neuroepithelioma cell line SK-N-MC. Here we show that this growth inhibition occurs in G_2. We show that bFGF is active on these cells during S and early G_2 phase. Therefore, this constitutes a rather unusual mechanism of growth inhibition, since it is generally believed that cells become refractory to extracellular signals after passage through the restriction point. In addition, we show that bFGF treatment inhibits Tyrl5 dephosphorylation of cdc2, similar to what is seen upon activation of the G_2 DNA damage checkpoint. Interestingly, both DNA damage- and bFGF-induced inhibition of cdc2-Tyr15 dephosphorylation can be reverted by caffeine. Taken together, these data define a growth factor sensitive point in G_2, that might act in a similar fashion as the G_2 DNA damage checkpoint.
机译:已显示碱性成纤维细胞生长因子(BFGF)诱导神经脑瘤细胞系SK-N-MC的生长抑制和细胞散射。 在这里,我们表明这种生长抑制在G_2中发生。 我们表明,在S和早期G_2相期间,BFGF在这些细胞上活跃。 因此,这构成了生长抑制的一种相当不寻常的机制,因为通常认为细胞在通过限制点之后对细胞对细胞外信号变得难治。 此外,我们表明,BFGF治疗抑制了CDC2的Tyrl5去磷酸化,类似于激活G_2 DNA损伤检查点后所见。 有趣的是,DNA损伤和BFGF诱导的CDC2-TYR15去磷酸化的抑制可以通过咖啡因再次恢复。 总之,这些数据定义了G_2中的生长因子敏感点,这可能以与G_2 DNA损伤检查点类似的方式起作用。

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