Abstract
The clinical benefit of heparin in cancer patients to prolong survival can be attributed to non-anticoagulant mechanisms. Since adhesion molecules are crucially involved in tumour cell metastasis, their inhibition offers an attractive approach for interfering with the metastatic cascade. Heparin is known to attenuate metastasis in a selectin-dependent manner and possesses a variety of additional effects that are thought to influence tumour cell dissemination, proliferation, and angiogenesis. We investigated the adhesion behaviour of B16F10 melanoma cells in vitro regarding selectin- and VLA-4/VCAM-1-mediated binding to get an insight into underlying mechanisms of melanoma cell metastasis. We show that B16F10 cells display binding ability to P- and L-selectin as well as to isolated platelets. In contrast, B16F10 cells did not adhere to immobilized P-selectin under flow. This contributes to recent findings that elucidate a major role of platelet P-selectin for microemboli formation and thus, facilitating metastasis. In contrast, B16F10 cells adhered to endothelial cells under flow, which could partly be inhibited by a function-blocking anti-VCAM-1 mAb. To emphasize VCAM-1 function, we analyzed cell adhesion at immobilized VCAM-1 ...Continue Reading
Citations
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