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Lung cancer is a severe disease threatening human health worldwide. Distanthematogenous metastasis results in poor prognosis and death of lung cancer patients.In the present study, we investigated the effect of circulatory platelets (PLTs)on hematogenous metastasis of non-small cell lung carcinoma (NSCLC). Laser scanningconfocal microscopy was employed to assay the expression of P-selectin in lungcancer tissue, paracancerous tissue and distant tissue, respectively. Meanwhile,fluorescence-activated cell sorting (FACS) was used to determine P-selectin activationin peripheral blood. Purified PLTs were co-cultured with A549 cells and humanvascular endothelial cells (HuvECs). Subsequently, the formation of PLT-lung cancercell complexes and their effects on rolling and adhesion of A549 on the surfaceof vascular endothelium were assayed. Integrin α3, α5, β1, ICAM-1 and VCAM-1 mRNAsand proteins were measured by reverse RT-PCR and western blot analysis, respectively.The expression of P-selectin in lung adenocarcinoma tissue was significantly strongercompared to that in paracancerous and distant tissues. P-selectin activation inperipheral blood in lung adenocarcinoma was markedly enhanced. The rolling rateof A549 on HuvECs was significantly slowed down after co-culture of activatedPLTs and A549 cells. The mRNA and protein levels of integrin α3, α5, β1, ICAM-1and VCAM-1 were significantly increased after the co-culture. In conclusion, thePLT-lung cancer cell complexes protected the lung cancer cells from mechanicalinjury under blood flow. Furthermore, up-regulated integrin α3, α5, β1 and endothelialcell adhesion molecules ICAM-1 and VCAM-1 promoted the adhesion of A549 on vascularendothelial cells, which may be responsible for hematogenous metastasis of lungcancer.

P-selectin-mediated platelet activation promotes adhesion of non-small cell lung carcinoma cells on vascular endothelial cells under flow