Hepatocyte growth factor induces delayed STAT3 phosphorylation through interleukin-6 expression.
作者： Bok-Soon Lee , Minseon Park , Hyun-Young Cha , Jae-Ho Lee
DOI: 10.1016/J.CELLSIG.2008.11.010
关键词:
摘要: Met receptor tyrosine kinase mediates pleiotropic cellular responses following its activation by hepatocyte growth factor or scatter (HGF/SF). STAT3 was reported to be one of direct downstream molecules in HGF/SF-Met signaling. In the present study, however, we observed that Tyr705 phosphorylated from 2 h 6 NIH3T3 and Chang liver cells, respectively, after HGF/SF treatment. Blocking phosphorylation cycloheximide actinomycin D rapid with conditioned medium HGF/SF-treated cells suggested a newly synthesized secretory protein responsible for delayed phosphorylation. Among known mediators induce phosphorylation, interleukin-6 (IL-6) mRNA were induced HGF/SF, released IL-6 accumulated Furthermore, neutralizing antibody abolished Treatment LY294002, PI3 inhibitor, but not other signal inhibitors, resulted loss showing involvement pathway. Collectively, these results demonstrate cascade stimulates production via pathway, leading as secondary effect.
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