中文摘要：

目的：研究P-选择素对黑色素瘤细胞整合素β1表达的影响,探讨P-选择素在肿瘤转移中的作用。方法：培养黑色素瘤细胞B16F10,在加或不加p38丝裂原活化蛋白激酶（MAPK）抑制剂SB203580的情况下,用P-选择素蛋白进行刺激,用蛋白质印迹（Western Blot）检测刺激后B16F10细胞整合素β1蛋白表达及p38 MAPK信号分子磷酸化水平的改变,用MTT法检测黏附细胞数目的变化。结果：P-选择素刺激B16F10细胞导致p38 MAPK磷酸化水平增高,整合素β1表达上调,用特异性阻断剂阻断p38 MAPK活化可以抑制P-选择素的诱导作用。MTT检测结果显示P-选择素刺激可增加细胞与整合素β1配基纤维粘连蛋白的黏附能力,说明细胞整合素β1表达增高。结论：P-选择素可以通过激活p38 MAPK途径诱导黑色素瘤B16F10细胞整合素β1的表达,提高肿瘤细胞的黏附能力,这可能是其促进肿瘤转移的机制之一。

英文摘要：

Objective： To investigate the effects of P-selectin on the expression of integrin β1 and the phosphorylation of p38 MAPK in melanoma cell line B16F10. Methods： B16F10 cells were treated with P-selectin in the presence or absence of SB203580, an inhibitor of p38 MAPK. The protein expression of integrin β1 and the phosphorylation level of p38 MAPK were determined by Western Blot. Cell adhesion was detected by MTT assay. Results： P-selectin significantly enhanced the expression of integrin β1 in B16F10 cells and the phosphorylation level of p38 MAPK. Inhibit p38 MAPK by SB203580 suppressed P-selectin-induced integrin β1 expression. Treated with P-selectin also enhanced the adhesion of B16F10 cells to fibronectin. Conclusion： P-selectin might effectively up-regulated integrin β1 expression in melanoma cells via p38 MAPK pathway, which may contribute, in part at least, to the tumor metastasis.