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 roles for VCAM-1 and Caveolin-1 in the regulation of metastatic potential of gastric tumor cells.
Original language | English |
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Pages (from-to) | 211-220 |
Number of pages | 10 |
Journal | Cellular Physiology and Biochemistry |
Volume | 17 |
Issue number | 5-6 |
DOIs | |
Publication status | Published - 2006 |
Keywords
- Caveolin-1
- Cell adhesion
- Gastric cancer
- Metastasis
- Vascular cell adhesion molecule-1
ASJC Scopus subject areas
- Physiology