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Effects of a glycogen synthase kinase‐3β inhibitor (LiCl) on c‐myc protein in intervertebral disc cells
Author(s) -
Hiyama Akihiko,
Sakai Daisuke,
Arai Fumiyuki,
Nakajima Daisuke,
Yokoyama Katsuya,
Mochida Joji
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23217
Subject(s) - wnt signaling pathway , microbiology and biotechnology , cell growth , viability assay , signal transduction , chemistry , lrp5 , cell , activator (genetics) , biology , biochemistry , gene
Abstract Wnt/β‐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. © 2011 Wiley‐Liss, Inc.