CD44：一种干性驱动、调节因子及标志物——集于一身？
CD44: a stemness driver, regulator, and marker-all in one?
DOI 原文链接
用sci-hub下载
如无法下载，请从 Sci-Hub 选择可用站点尝试。
影响因子:3.6
分区:医学3区 / 生物工程与应用微生物2区 细胞与组织工程3区 细胞生物学3区 血液学3区
发表日期:2024 Dec 06
作者:
Steffen J Sonnentag, Nagwa S M Ibrahim, Veronique Orian-Rousseau
DOI:
10.1093/stmcls/sxae060
摘要
尽管癌症干细胞的概念仍存在争议，但已有研究表明血液癌症以及部分实体瘤如结直肠癌在肿瘤发生和发展过程中依赖干细胞。此外，白血病如急性髓性白血病和结直肠癌的治疗抗药性，归因于一小部分具有干性特征的细胞群，称为微残留疾病（MRD）。本文回顾了癌症干细胞的发现及血液癌症研究在实体瘤中的平行贡献，特别关注CD44作为血液癌和多种实体瘤（尤其是胃肠道肿瘤）中的干细胞标志物。本文强调了CD44新近揭示的分子作用机制，表明其在干性、干细胞维持和耐药性中确实具有功能。我们试图建立CD44不同异构体在干性中的作用与其在肿瘤生长和转移特定步骤中的参与之间的联系。©作者所有，2024年由牛津大学出版社出版。若需商业再使用，请联系reprints@oup.com获取转载及译权。其他权限请通过我们网站文章页面的Permissions链接，使用RightsLink服务获得——详情请联系journals.permissions@oup.com。
Abstract
Although the concept of cancer stem cells is still controversial, previous studies have shown that blood cancers, as well as specific types of solid cancers such as colorectal cancer, rely on stem cells during the onset of tumor growth and further tumor development. Moreover, resistance to therapeutic treatment in leukemias such as acute myeloid leukemia and in colorectal cancer can be attributed to a small population of cells with stemness properties known as minimal residual disease. In this review, we look back on the discovery of cancer stem cells and the contribution of the findings in blood cancer to a parallel discovery in solid cancers. We focus on CD44 as a stem cell marker, both in blood cancers and in several types of solid cancers, particularly of the gastrointestinal tract. This review highlights newly discovered molecular mechanisms of action of CD44 which indicate that CD44 has indeed a function in stemness, stem cell maintenance, and drug resistance. We attempt here to make the link between the functions of CD44 isoforms in stemness and their involvement in specific steps of tumor growth and metastasis.© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.