Abstract |
The KAI1/CD82 protein has been documented as the tumor metastasis suppressor in many types of human cancers. KAI1/CD82 regulates cell motility and invasiveness; however, the mechanism by which this occurs remains to be fully established. Several studies have shown that KAI1/CD82 modulates integrin-dependent signaling. It was suggested that KAI1/CD82 might function to attenuate the beta1 integrin function of inducing cellular migration. A wound-healing and modified Boyden chamber assays were performed to investigate the mechanism of the KAI1/CD82-mediated inhibition of cell migration. It was found that the migratory ability of H1299/CD82 was inhibited. The immunoblotting and biotinylation assays revealed that H1299/CD82 showed significantly decreased expression of the mature form of beta1, which was functional at the cell surface. It was confirmed that KAI1/CD82 regulates the maturation of the beta1 integrin using CD82-specific si- RNA. These results support a model in which KAI1/CD82 attenuates the maturation of the beta1 integrin precursor and thereby suppresses cell migration.
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Authors | Bo Keun Jee, Joo Yong Lee, Young Lim, Kweon Haeng Lee, Yang-Hyeok Jo |
Journal | Biochemical and biophysical research communications
(Biochem Biophys Res Commun)
Vol. 359
Issue 3
Pg. 703-8
(Aug 03 2007)
ISSN: 0006-291X [Print] United States |
PMID | 17560548
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Integrin beta1
- Kangai-1 Protein
- RNA, Small Interfering
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Topics |
- Animals
- Cell Line
- Cell Membrane
(metabolism)
- Cell Movement
- Gene Expression Regulation, Neoplastic
- Glycosylation
- Humans
- Integrin beta1
(metabolism)
- Kangai-1 Protein
(genetics, metabolism)
- Lung Neoplasms
(genetics, metabolism, pathology)
- Mice
- Protein Processing, Post-Translational
- RNA, Small Interfering
(genetics)
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