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肿瘤内皮细胞在癌症进展中的作用。

Contribution of Tumor Endothelial Cells in Cancer Progression.

机构信息

Vascular Biology, Frontier Research Unit, Institute for Genetic Medicine, Hokkaido University, Sapporo 060-0815, Japan.

Department of Cardiovascular and Thoracic Surgery, Hokkaido University Graduate School of Medicine, Sapporo 060-0815, Japan.

出版信息

Int J Mol Sci. 2018 Apr 24;19(5):1272. doi: 10.3390/ijms19051272.


DOI:10.3390/ijms19051272
PMID:29695087
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5983794/
Abstract

Tumor progression depends on the process of angiogenesis, which is the formation of new blood vessels. These newly formed blood vessels supply oxygen and nutrients to the tumor, supporting its progression and providing a gateway for tumor metastasis. Tumor angiogenesis is regulated by the balance between angiogenic activators and inhibitors within the tumor microenvironment. Because the newly formed tumor blood vessels originate from preexisting normal vessels, tumor blood vessels, and tumor endothelial cells (TECs) have historically been considered to be the same as normal blood vessels and endothelial cells; however, evidence of TECs’ distinctive abnormal phenotypes has increased. In addition, it has been revealed that TECs constitute a heterogeneous population. Thus, TECs that line tumor blood vessels are important targets in cancer therapy. We have previously reported that TECs induce cancer metastasis. In this review, we describe recent studies on TEC abnormalities related to cancer progression to provide insight into new anticancer therapies.

摘要

肿瘤的进展取决于血管生成过程,即新血管的形成。这些新形成的血管为肿瘤提供氧气和营养,支持其进展,并为肿瘤转移提供门户。肿瘤血管生成受肿瘤微环境中血管生成激活剂和抑制剂之间的平衡调节。由于新形成的肿瘤血管来源于预先存在的正常血管,因此肿瘤血管和肿瘤内皮细胞(TEC)在历史上被认为与正常血管和内皮细胞相同;然而,TEC 具有独特异常表型的证据不断增加。此外,已经揭示 TEC 构成异质群体。因此,排列在肿瘤血管上的 TEC 是癌症治疗的重要靶点。我们之前曾报道 TEC 诱导癌症转移。在这篇综述中,我们描述了与癌症进展相关的 TEC 异常的最新研究,以期为新的抗癌治疗提供思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/0a4f3da23925/ijms-19-01272-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/8846050e5cfb/ijms-19-01272-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/f10ac21e1c91/ijms-19-01272-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/5c910694019f/ijms-19-01272-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/0a4f3da23925/ijms-19-01272-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/8846050e5cfb/ijms-19-01272-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/f10ac21e1c91/ijms-19-01272-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/5c910694019f/ijms-19-01272-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb53/5983794/0a4f3da23925/ijms-19-01272-g004.jpg

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本文引用的文献

[1]
Comprehensive in situ co-detection of aneuploid circulating endothelial and tumor cells.

Sci Rep. 2017-8-29

[2]
Endothelial Notch1 Activity Facilitates Metastasis.

Cancer Cell. 2017-2-23

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Identification of tumor endothelial cells with high aldehyde dehydrogenase activity and a highly angiogenic phenotype.

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