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- Title
a-1,3-Fucosyltransferase-VII stimulates the growth of hepatocarcinoma cells via the cyclin-dependent kinase inhibitor p27<sup>Kip1</sup>.
- Authors
Wang, Q. Y.; Guo, P.; Duan, L. L.; Shen, Z. H.; Chen, H. L.
- Abstract
After the transfection of a-1,3-fucosyltransferase (FucT)-VII cDNA into H7721 human hepatocarcinoma cells, the protein expression of some cyclins, cyclin-dependent kinases (CDKs) and cyclin-dependent kinase inhibitors (CDIs) p16INK4 and p21waf1/Cip1 were unchanged. However, CDI p27Kip1 protein, both the total amount and the amount that bound to CDK2, but not its mRNA, was significantly reduced. The de-inhibited CDK2 stimulated the phosphorylation of retinoblastoma (Rb) protein and facilitated the G1/S transition and growth rate of the cells. The decrease of p27Kip1 protein, the increase of CDK2 activity and Rb phosphorylation, as well as the cell growth and percentage of S phase cells were correlated to the increased amount of cell surface sialyl Lewis X (SLex) antigen in cells with different a-1,3-FucT-VII expression. The reduction in p27Kip1 and the difference in its expression among different transfected cells were blocked by the SLex antibody KM93 in a dose-dependent manner, indicating that p27Kip1 expression was influenced by a-1,3-FucT-VII and its product SLex. The MEK/MAPK signaling pathway was more important than the PI-3K pathway in the regulation of p27Kip1 expression.
- Subjects
FUCOSYLTRANSFERASES; CYCLINS; GROWTH factors; RETINOBLASTOMA; GENETIC regulation
- Publication
Cellular & Molecular Life Sciences, 2005, Vol 62, Issue 2, p171
- ISSN
1420-682X
- Publication type
Article
- DOI
10.1007/s00018-004-4349-8