Caveolin-1 is associated with VCAM-1 dependent adhesion of gastric cancer cells to endothelial cells
- Authors
- Shin, J (Shin, Jaeyoung); Kim, J (Kim, Jongmin); Ryu, B (Ryu, Byungkyu); Chi, SG (Chi, Sung-Gil); Park, H (Park, Heonyong)
- Issue Date
- Jul-2006
- Publisher
- KARGER
- Citation
- CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, v.17, no.5-6, pp 211 - 220
- Pages
- 10
- Journal Title
- CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
- Volume
- 17
- Number
- 5-6
- Start Page
- 211
- End Page
- 220
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/148676
- DOI
- 10.1159/000094126
- ISSN
- 1015-8987
1421-9778
- Abstract
- Background/Aims: Cell adhesion molecules play a critical role in the invasion and metastasis of a variety of human tumors. Abnormal expression of VCAM-1 has been demonstrated to correlate with the malignant progression of gastric tumors, but the molecular mechanism underlying the VCAM-1-dependent metastasis has been rarely investigated. To explore the role for tumor cell-expressing adhesion molecules in the carcinoma-endothelium adhesion, we analyzed expression status of adhesion molecules in gastric cancer cells and its association with tumor cell capability of endothelial adhesion. Methods: Endothelial adhesion ability of gastric tumor cells was tested using calcein AM staining assay. Expression of cell surface proteins was determined by Western blot, flow cytometry, and immunofluorescence assays. RNAi-mediated knockdown of gene expression and neutralization with specific antibodies were utilized for functional analysis. Results: One of three cell lines tested was identified to be adhesive to endothelial cells and express VCAM-1. Adherence ability of the cells was dramatically decreased by neutralization of surface VCAM-1. VCAM-1 was co-localized with Caveolin-1 and siRNA-mediated knockdown of Caveolin-1 expression significantly blocked the VCAM-1-dependent cell adhesion. Conclusions: Our data imply important
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