Nam Hyun-Ja, Kim Sujeong, Lee Min-Woo, Lee Bok-Soon, Hara Toshihiro, Saya Hideyuki, Cho Hyeseong, Lee Jae-Ho
Department of Biochemistry and Molecular Biology, Ajou University School of Medicine, South Korea.
Cell Signal. 2008 Jul;20(7):1349-58. doi: 10.1016/j.cellsig.2008.03.008. Epub 2008 Mar 21.
Growth factors accelerate G0 to S progression in the cell cycle, however, the roles of growth factors in other cell cycle phases are largely unknown. Here, we show that treatment of HeLa cells with hepatocyte growth factor (HGF) at G2 phase induced the G2/M transition delay as evidenced by FACS analysis as well as by mitotic index and time-lapse analyses. Growth factors such as epidermal growth factor (EGF) and fibroblast growth factor (FGF) also induced G2/M transition delay like HGF. HGF treatment at G2 phase causes a delayed activation of cyclin B1-associated kinase and a diminished nuclear translocation of cyclin B1. Either U0126, a MAPK kinase (MEK) inhibitor, or kinase-dead mutant of ribosomal S6 kinase (RSK) abolished the delay. Additionally, knockdown of RSK1, but not RSK2, with siRNA abrogated the delay, indicating that the extracellular-regulated protein kinase (ERK)-RSK1 mediates the HGF-induced delay. We further found that the delay in G2/M transition of cells expressing oncogenic HGF receptor, M1268T, was abolished by RSK1 knockdown. Intriguingly, we observed that HGF induced chromosomal segregation defects, and depletion of RSK1, but not RSK2, aggravated these chromosomal aberrations. Taken together, the ERK-RSK1 activation by growth factors delays G2/M transition and this might be required to maintain genomic integrity during growth factor stimulation.
生长因子可加速细胞周期中从G0期到S期的进程,然而,生长因子在细胞周期其他阶段的作用在很大程度上尚不清楚。在此,我们发现,在G2期用肝细胞生长因子(HGF)处理HeLa细胞会诱导G2/M期转换延迟,这通过流式细胞术分析、有丝分裂指数和延时分析得以证实。表皮生长因子(EGF)和成纤维细胞生长因子(FGF)等生长因子也像HGF一样诱导G2/M期转换延迟。在G2期用HGF处理会导致细胞周期蛋白B1相关激酶的激活延迟以及细胞周期蛋白B1的核转位减少。MAPK激酶(MEK)抑制剂U0126或核糖体S6激酶(RSK)的激酶失活突变体均可消除这种延迟。此外,用小干扰RNA(siRNA)敲低RSK1而非RSK2可消除这种延迟,这表明细胞外调节蛋白激酶(ERK)-RSK1介导了HGF诱导的延迟。我们进一步发现,敲低RSK1可消除表达致癌性HGF受体M1268T的细胞在G2/M期转换的延迟。有趣的是,我们观察到HGF会诱导染色体分离缺陷,而敲低RSK1而非RSK2会加剧这些染色体畸变。综上所述,生长因子激活ERK-RSK1会延迟G2/M期转换,这可能是在生长因子刺激期间维持基因组完整性所必需的。