Radhakrishnan Rangasudhagar, Ha Ji Hee, Dhanasekaran Danny N
Moffitt Cancer Center, 12902 Magnolia Drive, Tampa, FL 33612.
Genes Cancer. 2010 Oct;1(10):1033-43. doi: 10.1177/1947601910390516.
The gep oncogene, defined by the activated mutant of the α-subunit of the G protein G(12) (Gα(12)Q229L or Gα(12)QL), potently stimulates the proliferation of many different cell types in addition to inducing neoplastic transformation of several fibroblast cell lines. While it has been demonstrated that Gα(12)QL accelerates G1- to S-phase cell cycle progression, the precise mechanism through which Gα(12) communicates to cell cycle machinery is largely unknown. In the present study, we report that the activated-mutational as well as receptor-mediated-Gα(12) transmits its proliferative signals to cell cycle machinery by modulating the levels of the S-phase kinase-associated protein 2 (Skp2), an E3 ubiquitin ligase, involved in the regulation of the cyclin-dependent kinase inhibitor (CKI), p27(Kip1). Our results show that the expression of Gα(12)QL leads to an increase in the levels of Skp2 with a correlatable decrease in p27(Kip1) levels and subsequent increase in the activities of specific CDKs. By demonstrating that the transient expression of Gα(12)QL induces an increase in Skp2 levels with resultant downregulation of p27(Kip1) in both NIH3T3 and human astrocytoma 1321N1 cells, we establish here that the effect of Gα(12) on Skp2/p27(Kip1) is cell type independent. In addition, we demonstrate that LPA-stimulated proliferation and changes in Skp2 and p27(Kip1) levels in 1321N1 cells could be inhibited by the expression of a dominant-negative mutant of Gα(12), thereby pointing to the critical role of Gα(12) in LPA-mediated mitogenic signaling. Our findings also indicate that LPA as well as Gα(12)-mediated upregulation of Skp2 requires a yet to be characterized mechanism involving JNK. Since Skp2 has been identified as an oncogene, and it is overexpressed in many cancers, our results presented here describe for the first time that Skp2 is a novel target in the cell cycle machinery through which Gα(12) and its cognate receptors transmit their oncogenic signals.
由G蛋白G(12)的α亚基(Gα(12)Q229L或Gα(12)QL)的激活突变体所定义的Gep癌基因,除了诱导几种成纤维细胞系发生肿瘤转化外,还能有效刺激多种不同细胞类型的增殖。虽然已经证明Gα(12)QL能加速细胞从G1期到S期的细胞周期进程,但Gα(12)与细胞周期机制沟通的精确机制在很大程度上尚不清楚。在本研究中,我们报告激活突变型以及受体介导的Gα(12)通过调节S期激酶相关蛋白2(Skp2)的水平,将其增殖信号传递给细胞周期机制,Skp2是一种E3泛素连接酶,参与细胞周期蛋白依赖性激酶抑制剂(CKI)p27(Kip1)的调控。我们的结果表明,Gα(12)QL的表达导致Skp2水平升高,p27(Kip1)水平相应降低,随后特定周期蛋白依赖性激酶(CDK)的活性增加。通过证明Gα(12)QL的瞬时表达在NIH3T3细胞和人星形细胞瘤1321N1细胞中均诱导Skp2水平升高,导致p27(Kip1)下调,我们在此确定Gα(12)对Skp2/p27(Kip1)的影响与细胞类型无关。此外,我们证明,Gα(12)的显性负突变体的表达可抑制溶血磷脂酸(LPA)刺激的1321N1细胞增殖以及Skp2和p27(Kip1)水平的变化,从而表明Gα(12)在LPA介导的促有丝分裂信号传导中起关键作用。我们的研究结果还表明,LPA以及Gα(12)介导的Skp2上调需要一种尚未明确的涉及JNK的机制。由于Skp2已被鉴定为一种癌基因,且在许多癌症中过度表达,我们在此展示的结果首次描述了Skp2是细胞周期机制中的一个新靶点,Gα(12)及其同源受体通过该靶点传递致癌信号。