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[E-selectin mediates early adhesion of HepG2 hepatoma cells to endothelial cells]
1Liver Cancer Institute, Zhongshan Hospital, Shanghai Medical University, Shanghai 200032, China.
Objective:
To study the role of E-selectin and sLe(x) in the adhesion between hepatoma cells (HepG2) and endothelial cells, and to select drugs capable of inhibiting such adhesion.
Methods:
HepG2 cells were vitally stained with fluorescent dye BCECF-AM. Adhesion between the fluorescent HepG2 cells and human umbilical vein endothelial cells (HUVEC) was examined by solid phase adhesion assay in vitro. A number of agents were tested for their effect on the tumor cell-endothelial adhesion.
Results:
sLe(x) on the surface of HepG2 cells and E-selectin expressed on the surface of HUVEC were necessary for early adhesion. HepG2 cells could activate HUVEC to increase their adhesiveness to HepG2 cells. Dexamethasone, phenylarsenic oxide, levamisole and actinomycin D were able to block the adhesion between HepG2 to HUVEC at low concentrations.
Conclusion:
sLe(x) and E-selectin are important molecules in the early adhesion of hepatoma cells to HUVEC. Cytokine-like factors of HepG2 origin are likely involved in the activation of endothelial cells in the target tissue. Agents capable of inhibiting NF kappa B can be hopefuly used as anti-adhesion drugs to inhibit metastasis of liver cancer.