| First Author | Qi CL | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 3 | Pages | e91320 |
| PubMed ID | 24632801 | Mgi Jnum | J:215115 |
| Mgi Id | MGI:5604676 | Doi | 10.1371/journal.pone.0091320 |
| Citation | Qi CL, et al. (2014) P-selectin-mediated platelet adhesion promotes the metastasis of murine melanoma cells. PLoS One 9(3):e91320 |
| abstractText | Studies have indicated that the aggregation of activated platelets with cancer cells facilitates tumor metastasis; the adhesion molecule P-selectin may be an important mediator of this process, but the detailed mechanism is unclear. In the current study, we established a B16F10 (B16) cell metastatic model in P-selectin knockout (P-sel-/-) mice to determine the effect of P-selectin-mediated platelet adhesion on metastasis. Compared with C57 mice, P-sel-/- mice developed fewer metastatic foci, and cell proliferation within the metastatic tumors was inhibited by P-selectin deficiency. The platelet refusion assay demonstrated that mice with P-sel-/- platelets developed fewer lung metastatic foci (P<0.01) with a lower microvascular density (MVD) than mice with wild-type platelets. A co-culture model of platelets and B16 cells was utilized to determine the difference in VEGF concentration in the supernatants. The results demonstrated that the supernatant from the P-sel-/- platelet/B16 co-culture had a lower concentration of VEGF. Therefore, our findings indicated that P-selectin deficiency inhibited the metastasis of B16 cells and that wild-type platelet refusion reversed this inhibition. The P-selectin-mediated interaction between platelets and B16 cells promoted angiogenesis by up-regulating VEGF. |
