School of Pharmacy, University of East Anglia, Norwich, UK.
Cell Biochem Funct. 2013 Jun;31(4):312-8. doi: 10.1002/cbf.2901. Epub 2012 Sep 14.
Chemokine receptors induce cell migration, but the molecular basis of the signal cascade involved is not completely understood. Therefore, we investigated here the molecular mechanisms of CCL3-, CCL5- and CCL8-induced cells migration and investigated whether the Janus kinase/signal transducer and activator of transcription (STAT) signalling pathway is involved. Some STAT3 inhibitors, like Cucurbitacin I, destroy the actin cytoskeleton inside the cells and therefore prevent any cellular migration. However, for inhibitors that do not affect the actin cytoskeleton or induce cell death, we show that chemokine-induced cell migration is not dependent on activation of Janus kinase 2 or STAT3.
趋化因子受体诱导细胞迁移，但涉及的信号级联的分子基础尚不完全清楚。因此，我们在这里研究了 CCL3、CCL5 和 CCL8 诱导细胞迁移的分子机制，并研究了 Janus 激酶/信号转导和转录激活因子 (STAT) 信号通路是否参与其中。一些 STAT3 抑制剂，如葫芦素 I，会破坏细胞内的肌动蛋白细胞骨架，从而阻止任何细胞迁移。然而，对于不影响肌动蛋白细胞骨架或诱导细胞死亡的抑制剂，我们表明趋化因子诱导的细胞迁移不依赖于 Janus 激酶 2 或 STAT3 的激活。
