Activation of the IGF-II Gene by HBV-X Protein Requires PKC and p44/p42 Map Kinase Signalings

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Title
Activation of the IGF-II Gene by HBV-X Protein Requires PKC and p44/p42 Map Kinase Signalings
Author(s)
Suk Mi Kang-Park; Je Ho Lee; Jeh Hoon Shin; Young Ik Lee
Bibliographic Citation
Biochemical and Biophysical Research Communications, vol. 283, no. 2, pp. 303-307
Publication Year
2001
Abstract
We have recently shown that HBx protein, one of the causative agents of hepatocellular carcinomas, regulates Sp1 mediated transcription of insulin-like growth factor II promoter 4 (Lee et al. (1998) Oncogene 16, 2367-2380). Here we show that PKC and p44/p42MAPK signalings are required for the HBx-induced Sp1-mediated IGF-II P4 transcriptional activity since (i) PKC activation by PMA or PKC expression vector increases Sp1 phosphorylation and P4 activity in HBx-transfected HepG2 cells; (ii) PKC inhibition by PKC inhibitor G?6976 reduces Spl phosphorylation, P4 activity, and IGF-II mRNA in HBx-transfected HepG2 cells; and (iii) the inhibition of MEK activation by U0126 reduces Sp1 phosphorylation, P4 activity and IGF-II mRNA in HBx-transfected HepG2 cells. These results demonstrate that PKC and p44/p42 MAPK cascades are the essential signaling pathways in Sp1-mediated IGF-II gene activation by HBx.
Keyword
HBV-XHepatocellular carcinomasIGF-IIMAPKPhosphorylationPKCSp1
ISSN
0006-291X
Publisher
Elsevier
DOI
http://dx.doi.org/10.1006/bbrc.2001.4767
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
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