基因沉默
医学
乳腺癌
癌症
转移
癌症研究
纤维蛋白
抗凝血酶
肿瘤进展
免疫学
病理
内科学
肝素
生物
生物化学
基因
作者
Jeroen T. Buijs,Betül Ünlü,El Houari Laghmani,Marco Heestermans,Bart J.M. van Vlijmen,Henri H. Versteeg
标识
DOI:10.1016/j.thromres.2022.11.018
摘要
Local coagulation activation has been shown to impact both primary tumor growth and metastasis in mice. It is well known that components of the blood clotting cascade such as tissue factor and thrombin play a role in tumor progression by activating cellular receptors and local formation of fibrin. However, whether venous thromboembolism (VTE) or a hypercoagulable state has a direct impact on cancer progression is unknown. Here we have combined an orthotopic murine breast cancer model, using female Nod-SCID mice, with siRNA-mediated silencing of antithrombin (siAT) leading to the induction of a systemic hypercoagulable state. We show that, compared to control siRNA-treated (not experiencing a hypercoagulable state) tumor-bearing mice, siAT treated tumor-bearing mice do not show enhanced tumor growth nor enhanced metastasis. We conclude that, in this murine model for hypercoagulability, induction of a hypercoagulable state does not contribute to breast cancer progression.
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