Effects of a Glycogen Synthase Kinase-3β Inhibitor (LiCl) on c-myc Protein in Intervertebral Disc Cells
Effects of a Glycogen Synthase Kinase-3β Inhibitor (LiCl) on c-myc Protein in Intervertebral Disc Cells
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DOI：
10.1002/jcb.23217
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发表时间：
2011-10-01
影响因子：
4
通讯作者：
Mochida, Joji
中科院分区：
文献类型：
--
作者：
Hiyama, Akihiko;Sakai, Daisuke;Mochida, Joji
Wnt/β-连环蛋白（以下称为Wnt）信号传导是关节发育的关键诱导剂和调节剂，并且参与骨和软骨的形成。我们以前报道过Wnt信号在椎间盘细胞增殖和细胞衰老的控制中起着至关重要的作用。在本研究中，我们提供的证据表明，c-myc，细胞增殖所需的关键蛋白质的表达，是由Wnt信号调节。我们的数据还表明，激活Wnt信号的LiCl，Wnt信号激活剂，导致抑制c-myc启动子的活性和表达。为了确定Wnt信号是否调节c-myc的表达，我们测量了其转录和蛋白表达。用LiCl处理后，c-myc的表达在mRNA和蛋白水平上都受到抑制。在用c-myc处理的髓核细胞中，细胞活力显著增加，而用c-myc抑制剂处理降低细胞活力。综上所述，这些结果表明，c-myc是一个重要的因素，促进髓核细胞增殖。这些发现为髓核细胞增殖的调控和维持提供了新的见解。J.细胞。112：2974-2986，2011. (C)2011 Wiley-Liss，Inc.
Wnt/beta-catenin (hereafter called Wnt) signaling is a key inducer and regulator of joint development, and is involved in the formation of bone and cartilage. We previously reported that Wnt signaling plays an essential role in the control of cell proliferation and cell senescence in intervertebral disc cells. In the present study, we provide evidence that the expression of c-myc, a key protein required for cell proliferation, is regulated by Wnt signaling. Our data also show that activation of Wnt signaling by LiCl, a Wnt signaling activator, leads to the suppression of c-myc promoter activity and expression. To ascertain whether Wnt signaling regulates the expression of c-myc, we measured both its transcript and protein expression. Following treatment with LiCl, c-myc expression was suppressed at both the mRNA and protein levels. In nucleus pulposus cells treated with c-myc, cell viability increased significantly, whereas treatment with a c-myc inhibitor decreased cell viability. Taken together, these results suggest that c-myc is an important factor that promotes the proliferation of nucleus pulposus cells. These findings provide new insight into the regulation and maintenance of cell proliferation in nucleus pulposus cells. J. Cell. Biochem. 112: 2974-2986, 2011. (C) 2011 Wiley-Liss, Inc.