The role of podoplanin in tumor-associated thrombosis

A. V. Savelyeva, K. A. Pishchulov
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Abstract

Venous thromboembolism (VTE) is highly consequential for patients with cancer, it is the second leading cause of death in these patients. The literature describes several mechanisms leading to these complications. One of these is the interaction of podoplanin (PDPN), which is the subject of this article, with its receptor on platelets CLEC-2 (C-type lectin-like type II transmembrane receptor). This interaction leads to platelet activation and promotes hematogenous metastasis and thrombosis associated with cancer. Podoplanin is expressed in gliomas, squamous cell carcinoma, osteosarcoma by cancer cells, and it is also normally expressed in podocytes and lymphatic endothelial cells, but not in vascular endothelium. Thrombus inflammation initiates ectopic expression of podoplanin in vascular endothelial cells, which promotes thrombosis. It has been shown that podoplanin expression correlates with the incidence of VTE, as well as with cancer metastasis. Violation of the PDPN-CLEC-2 interaction may become a new direction in the development of drugs for the prevention of thrombosis for patients with cancer.
足多planin在肿瘤相关血栓中的作用
静脉血栓栓塞(VTE)对癌症患者的影响很大,是癌症患者死亡的第二大原因。文献描述了导致这些并发症的几种机制。其中之一是podoplanin (PDPN),这是本文的主题,与其在血小板上的受体clc -2 (c型凝集素样II型跨膜受体)的相互作用。这种相互作用导致血小板活化,促进与癌症相关的血液转移和血栓形成。Podoplanin在胶质瘤、鳞状细胞癌、骨肉瘤等肿瘤细胞中均有表达,通常在足细胞和淋巴内皮细胞中也有表达,但在血管内皮中不表达。血栓炎症引发血管内皮细胞中podoplanin的异位表达,从而促进血栓形成。已有研究表明,podoplanin的表达与静脉血栓栓塞的发生率以及肿瘤转移有关。破坏PDPN-CLEC-2相互作用可能成为癌症患者预防血栓形成药物开发的新方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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