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醛脱氢酶作为实体瘤转移的标志物和功能介质。

Aldehyde dehydrogenase as a marker and functional mediator of metastasis in solid tumors.

作者信息

Rodriguez-Torres Mauricio, Allan Alison L

机构信息

London Regional Cancer Program, London Health Sciences Centre, London, ON, Canada.

Department of Anatomy & Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada.

出版信息

Clin Exp Metastasis. 2016 Jan;33(1):97-113. doi: 10.1007/s10585-015-9755-9. Epub 2015 Oct 7.

DOI:10.1007/s10585-015-9755-9
PMID:26445849
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4740561/
Abstract

There is accumulating evidence indicating that aldehyde dehydrogenase (ALDH) activity selects for cancer cells with increased aggressiveness, capacity for sustained proliferation, and plasticity in primary tumors. However, emerging data also suggests an important mechanistic role for the ALDH family of isoenzymes in the metastatic activity of tumor cells. Recent studies indicate that ALDH correlates with either increased or decreased metastatic capacity in a cellular context-dependent manner. Importantly, it appears that different ALDH isoforms support increased metastatic capacity in different tumor types. This review assesses the potential of ALDH as biological marker and mechanistic mediator of metastasis in solid tumors. In many malignancies, most notably in breast cancer, ALDH activity and expression appears to be a promising marker and potential therapeutic target for treating metastasis in the clinical setting.

摘要

越来越多的证据表明,醛脱氢酶(ALDH)活性会选择原发性肿瘤中具有更高侵袭性、持续增殖能力和可塑性的癌细胞。然而,新出现的数据也表明,ALDH同工酶家族在肿瘤细胞的转移活性中具有重要的机制作用。最近的研究表明,在细胞背景依赖的方式下,ALDH与转移能力的增加或降低相关。重要的是,不同的ALDH同工型似乎在不同的肿瘤类型中支持转移能力的增加。这篇综述评估了ALDH作为实体瘤转移的生物标志物和机制介质的潜力。在许多恶性肿瘤中,最显著的是在乳腺癌中,ALDH活性和表达似乎是临床环境中治疗转移的一个有前景的标志物和潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e6a/4740561/95adfa456e21/10585_2015_9755_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e6a/4740561/95adfa456e21/10585_2015_9755_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e6a/4740561/95adfa456e21/10585_2015_9755_Fig1_HTML.jpg

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