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膀胱癌患者血清中巨噬细胞移动抑制因子-抗凝血酶 III 复合物减少:复合物形成作为失活机制。

Macrophage migration inhibitory factor anti-thrombin III complexes are decreased in bladder cancer patient serum: Complex formation as a mechanism of inactivation.

机构信息

Bay Pines VA Healthcare System, Research and Development, Bay Pines, FL 33744, USA.

出版信息

Cancer Lett. 2010 Apr 1;290(1):49-57. doi: 10.1016/j.canlet.2009.08.025. Epub 2009 Sep 16.

DOI:10.1016/j.canlet.2009.08.025
PMID:19762145
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2832085/
Abstract

Mounting evidence suggests that the pro-inflammatory cytokine macrophage migration inhibitory factor (MIF) may serve as an important link between chronic inflammation and carcinogenesis as evidenced by the increase in serum MIF found in patients with various cancers. The present study identifies anti-thrombin III (ATIII) as an endogenous MIF binding protein, which reduces MIF biological activity. Serum MIF in bladder cancer patients (TCC stage II, n=50) was increased when compared to normal patients (n=50), while ATIII-MIF complexes were decreased in bladder cancer patient serum. These data suggest that increased circulating levels of bioactive MIF are present in bladder cancer patient serum.

摘要

越来越多的证据表明,促炎细胞因子巨噬细胞移动抑制因子(MIF)可能是慢性炎症与癌变之间的重要联系,这表现在各种癌症患者血清中发现的 MIF 水平升高。本研究发现抗凝血酶 III(ATIII)是 MIF 的内源性结合蛋白,可降低 MIF 的生物学活性。与正常患者(n=50)相比,膀胱癌患者(TCC Ⅱ期,n=50)的血清 MIF 增加,而膀胱癌患者血清中的 ATIII-MIF 复合物减少。这些数据表明,膀胱癌患者血清中存在循环生物活性 MIF 水平升高。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/6137e94dfb00/nihms146096f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/c140a589ddc5/nihms146096f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/82f8f5ffa9db/nihms146096f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/d281ef7d8eb1/nihms146096f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/153b22db1e94/nihms146096f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/6137e94dfb00/nihms146096f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/c140a589ddc5/nihms146096f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/82f8f5ffa9db/nihms146096f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/d281ef7d8eb1/nihms146096f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/153b22db1e94/nihms146096f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd13/2832085/6137e94dfb00/nihms146096f5.jpg

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本文引用的文献

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Mediators Inflamm. 2009;2009:535348. doi: 10.1155/2009/535348. Epub 2009 Mar 22.
2
A tautomerase-null macrophage migration-inhibitory factor (MIF) gene knock-in mouse model reveals that protein interactions and not enzymatic activity mediate MIF-dependent growth regulation.一种缺乏互变异构酶的巨噬细胞迁移抑制因子(MIF)基因敲入小鼠模型显示,是蛋白质相互作用而非酶活性介导了MIF依赖的生长调节。
Mol Cell Biol. 2009 Apr;29(7):1922-32. doi: 10.1128/MCB.01907-08. Epub 2009 Feb 2.
3
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