Takano T, Takada K, Tada H, Nishiyama S, Amino N
Department of Laboratory Medicine, Osaka University School of Medicine, Japan.
Biochem Biophys Res Commun. 1993 Feb 15;190(3):801-7. doi: 10.1006/bbrc.1993.1120.
IGF-I, when added to TSH-primed FRTL-5 cells, induces a long lasting Ca2+ influx and then DNA synthesis. Ca2+ channel agonist, BAYK 8644, is capable to mimic these effects on cell proliferation. We studied the effect of genistein, a specific tyrosine kinase inhibitor, on BAY K8644- or IGF-I- induced cell cycle progression in FRTL-5 cells. Genistein inhibited DNA synthesis induced by BAY K8644 and by IGF-I. In contrast, Ca2+ influx stimulated by BAY K8644 was not inhibited. These data demonstrate that the signal transduction pathway induced by BAY K8644 or IGF-I may possibly involve genistein-sensitive process at the downstream step of Ca2+ entry.
将胰岛素样生长因子-I（IGF-I）添加到经促甲状腺激素（TSH）预处理的FRTL-5细胞中时，会诱导持久的钙离子内流，随后引发DNA合成。钙离子通道激动剂BAYK 8644能够模拟这些对细胞增殖的影响。我们研究了染料木黄酮（一种特异性酪氨酸激酶抑制剂）对BAY K8644或IGF-I诱导的FRTL-5细胞周期进程的影响。染料木黄酮抑制了BAY K8644和IGF-I诱导的DNA合成。相比之下，BAY K8644刺激的钙离子内流未受到抑制。这些数据表明，BAY K8644或IGF-I诱导的信号转导途径可能在钙离子内流的下游步骤涉及对染料木黄酮敏感的过程。
