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表达组织因子的肿瘤细胞在体外静态和剪切条件下可与固定化的重组组织因子途径抑制剂结合。

Tissue factor-expressing tumor cells can bind to immobilized recombinant tissue factor pathway inhibitor under static and shear conditions in vitro.

作者信息

Che Sara P Y, DeLeonardis Christine, Shuler Michael L, Stokol Tracy

机构信息

Department of Biomedical Engineering, College of Engineering, Cornell University, Ithaca, NY, United States of America.

Department of Population Medicine and Diagnostic Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, United States of America.

出版信息

PLoS One. 2015 Apr 7;10(4):e0123717. doi: 10.1371/journal.pone.0123717. eCollection 2015.

Abstract

Mammary tumors and malignant breast cancer cell lines over-express the coagulation factor, tissue factor (TF). High expression of TF is associated with a poor prognosis in breast cancer. Tissue factor pathway inhibitor (TFPI), the endogenous inhibitor of TF, is constitutively expressed on the endothelium. We hypothesized that TF-expressing tumor cells can bind to immobilized recombinant TFPI, leading to arrest of the tumor cells under shear in vitro. We evaluated the adhesion of breast cancer cells to immobilized TFPI under static and shear conditions (0.35 - 1.3 dyn/cm2). We found that high-TF-expressing breast cancer cells, MDA-MB-231 (with a TF density of 460,000/cell), but not low TF-expressing MCF-7 (with a TF density of 1,400/cell), adhered to recombinant TFPI, under static and shear conditions. Adhesion of MDA-MB-231 cells to TFPI required activated factor VII (FVIIa), but not FX, and was inhibited by a factor VIIa-blocking anti-TF antibody. Under shear, adhesion to TFPI was dependent on the TFPI-coating concentration, FVIIa concentration and shear stress, with no observed adhesion at shear stresses greater than 1.0 dyn/cm2. This is the first study showing that TF-expressing tumor cells can be captured by immobilized TFPI, a ligand constitutively expressed on the endothelium, under low shear in vitro. Based on our results, we hypothesize that TFPI could be a novel ligand mediating the arrest of TF-expressing tumor cells in high TFPI-expressing vessels under conditions of low shear during metastasis.

摘要

乳腺肿瘤和恶性乳腺癌细胞系过度表达凝血因子组织因子(TF)。TF的高表达与乳腺癌的不良预后相关。组织因子途径抑制剂(TFPI)是TF的内源性抑制剂,在内皮细胞上组成性表达。我们推测,表达TF的肿瘤细胞可以与固定化的重组TFPI结合,导致肿瘤细胞在体外剪切力作用下停滞。我们评估了乳腺癌细胞在静态和剪切条件(0.35 - 1.3达因/平方厘米)下与固定化TFPI的粘附情况。我们发现,高表达TF的乳腺癌细胞MDA-MB-231(TF密度为460,000/细胞),而不是低表达TF的MCF-7(TF密度为1,400/细胞),在静态和剪切条件下均能粘附于重组TFPI。MDA-MB-231细胞与TFPI的粘附需要活化的因子VII(FVIIa),而不是FX,并且被一种阻断FVIIa的抗TF抗体所抑制。在剪切力作用下,与TFPI的粘附取决于TFPI包被浓度、FVIIa浓度和剪切应力,在剪切应力大于1.0达因/平方厘米时未观察到粘附现象。这是第一项表明表达TF的肿瘤细胞可以在体外低剪切力条件下被固定化的TFPI捕获的研究,TFPI是在内皮细胞上组成性表达的一种配体。基于我们的结果,我们推测TFPI可能是一种新型配体,在转移过程中低剪切力条件下介导表达TF的肿瘤细胞在高表达TFPI的血管中停滞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd7a/4388665/5107a0aec378/pone.0123717.g001.jpg

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