TGF-beta-induced cell-cycle arrest through the p21(WAF1)/(CIP1)-G1 cyclin/Cdks-p130 pathway in gastric-carcinoma cells
- Authors
- Yoo, YD; Choi, JY; Lee, SJ; Kim, JS; Min, BR; Lee, YI; Kang, YK
- Issue Date
- 12-Nov-1999
- Publisher
- WILEY
- Citation
- INTERNATIONAL JOURNAL OF CANCER, v.83, no.4, pp 512 - 517
- Pages
- 6
- Indexed
- SCIE
SCOPUS
- Journal Title
- INTERNATIONAL JOURNAL OF CANCER
- Volume
- 83
- Number
- 4
- Start Page
- 512
- End Page
- 517
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/23721
- DOI
- 10.1002/(SICI)1097-0215(19991112)83:4<512::AID-IJC13>3.0.CO;2-Z
- ISSN
- 0020-7136
1097-0215
- Abstract
- Transforming growth factor-beta 1 (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-P 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. Int. J. Cancer 83:512-517, 1999. (C) 1999 Wiley-Liss, Inc.
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Collections - 3. Graduate School > Biomedical Research Center > 1. Journal Articles
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