Integrin beta1 subunit overexpressed in the SMMC-7721 cells regulates the promoter activity of p21(CIP1) and enhances its transcription.

Abstract

Evidence has been emerging to suggest that integrin could induce growth inhibition in some cell types. Some of the molecular mechanisms underlying growth arrest have been elucidated. We reported here that overexpression of integrin beta1 imposed a growth inhibitory effect on the hepatocellular carcinoma cell line SMMC-7721, and this phenomenon was mainly attributed to the cyclin-dependent kinase inhibitor p21(CIP1). Furthermore, our findings suggested that transcription activity of the p21(CIP1) gene could be upregulated in the integrin beta1-overexpressing cells, and possibly controlled by the cis-elements in the core region of the p21(CIP1) promoter.

• Authors: Yu-Long Liang, Yi Fu, Si-Gang Chen, Xiu-Mei Cai, Jian-Min Su, Jia-Wei Jin, Dong-Zhu Ma, Zeng-Xia Li, Wen Zhang, Xiliang Zha
• Journal: FEBS letters (FEBS Lett) Vol. 558 Issue 1-3 Pg. 107-13 (Jan 30 2004) ISSN: 0014-5793 [Print] England
• PMID: 14759525 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• CDKN1A protein, human
• Cyclin-Dependent Kinase Inhibitor p21
• Cyclins
• Integrin beta1

Topics

• Base Sequence
• Binding Sites
• Carcinoma, Hepatocellular
• Cell Division
• Cell Line, Tumor
• Cell Survival
• Cyclin-Dependent Kinase Inhibitor p21
• Cyclins (genetics, metabolism)
• Gene Expression Regulation, Neoplastic
• Humans
• Integrin beta1 (metabolism)
• Liver Neoplasms (metabolism)
• Mutation
• Promoter Regions, Genetic
• Transcription, Genetic
• Transcriptional Activation