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首页> 外文期刊>Cancer science. >Platelets and fibrinogen facilitate each other in protecting tumor cells from natural killer cytotoxicity.
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Platelets and fibrinogen facilitate each other in protecting tumor cells from natural killer cytotoxicity.

机译:血小板和纤维蛋白原在保护肿瘤细胞免受自然杀伤细胞毒性方面相互促进。

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摘要

The functions of platelets and fibrinogen in protecting tumor cells from natural killer cytotoxicity have been discussed for more than 20 years. However, their exact roles and relationships in the process are still not clear. In this study, we show that tumor cells prefer to adhere to fibrinogen than to platelets, and fibrinogen can enhance the adhesion of tumor cells to platelets. Beta3 integrin plays an important role in the adhesion of B16F10 to platelets enhanced by fibrinogen. In the presence of thrombin, fibrinogen forms dense fibrin(ogen) layers around tumor cells. Tumor cells can induce platelets to aggregate and form thrombin. Platelets, as well as thrombin, can help fibrinogen protect tumor cells from lethal contact with natural killer cells and natural killer cytotoxicity. Hirudin, a specific inhibitor of thrombin, can reverse the effect of platelets on fibrinogen in blocking natural killer cytotoxicity. Our results suggest that fibrinogen helps platelets to adhere to tumor cells, and platelets in turn promote more fibrinogen to aggregate around tumor cells by forming thrombin. They facilitate each other in protecting tumor cells from natural killer cytotoxicity.
机译:血小板和纤维蛋白原在保护肿瘤细胞免受自然杀伤细胞毒性方面的功能已经讨论了20多年。但是,它们在过程中的确切角色和关系仍然不清楚。在这项研究中,我们表明肿瘤细胞比纤维蛋白原更倾向于粘附到纤维蛋白原上,而纤维蛋白原可以增强肿瘤细胞对血小板的粘附。 Beta3整合素在B16F10与纤维蛋白原增强的血小板的粘附中起重要作用。在凝血酶存在下,纤维蛋白原在肿瘤细胞周围形成致密的纤维蛋白(原)层。肿瘤细胞可诱导血小板聚集并形成凝血酶。血小板以及凝血酶可以帮助纤维蛋白原保护肿瘤细胞免于与自然杀伤细胞的致命接触和自然杀伤细胞的细胞毒性。水rud素是凝血酶的一种特异性抑制剂,可以逆转血小板对纤维蛋白原的作用,从而阻断自然杀伤细胞的细胞毒性。我们的结果表明,纤维蛋白原有助于血小板粘附于肿瘤细胞,而血小板又通过形成凝血酶促进更多的纤维蛋白原聚集在肿瘤细胞周围。它们在保护肿瘤细胞免受自然杀伤细胞毒性方面相互促进。

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