| Literature DB >> 10508488 |
Y D Yoo1, J Y Choi, S J Lee, J S Kim, B R Min, Y I Lee, Y K Kang.
Abstract
Transforming growth factor-beta1 (TGF-beta) inhibits cell-cycle progression of many types of cells by arresting them in G(1)/S phase through inhibition of the active cyclin-Cdk complexes that lead to inhibition of Rb phosphorylation. In gastric-cancer cells, SNU16, TGF-beta treatment induced enhanced expression of p21(WAF1/CIP1) (p21), which inhibited the kinase activity of cyclin-D- and cyclin-E-associated Cdks and blocked p130 phosphorylation. TGF-beta also enhanced the stability of p130, suggesting that hypophosphorylation of p130 and increased stability of p130 contribute to p130-mediated G(1) arrest in gastric-cancer cells. Our results demonstrate that p21 and p130 are major downstream targets of TGF-beta in gastric-cancer cells and that a p21-G(1) cyclin/Cdks-p130/E2F pathway mediates growth inhibition by TGF-beta in these cells. Copyright 1999 Wiley-Liss, Inc.Entities:
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Year: 1999 PMID： 10508488 DOI： 10.1002/(sici)1097-0215(19991112)83:4<512::aid-ijc13>3.0.co;2-z
Source DB: PubMed Journal: Int J Cancer ISSN： 0020-7136 Impact factor: 7.396