当前位置: X-MOL 学术Glycobiology › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Galectin-3 and cancer stemness
Glycobiology ( IF 3.4 ) Pub Date : 2018-01-05 , DOI: 10.1093/glycob/cwy001
Pratima Nangia-Makker 1, 2 , Victor Hogan 1 , Avraham Raz 1, 2, 3
Affiliation  

Over the last few decades galectin-3, a carbohydrate binding protein, with affinity for N-acetyllactosamine residues, has been unique due to the regulatory roles it performs in processes associated with tumor progression and metastasis such as cell proliferation, homotypic/heterotypic aggregation, dynamic cellular transformation, migration and invasion, survival and apoptosis. Structure–function association of galectin-3 reveals that it consists of a short amino terminal motif, which regulates its nuclear-cytoplasmic shuttling; a collagen α-like domain, susceptible to cleavage by matrix metalloproteases and prostate specific antigen; accountable for its oligomerization and lattice formation, and a carbohydrate-recognition/binding domain containing the anti-death motif of the Bcl2 protein family. This structural complexity permits galectin-3 to associate with numerous molecules utilizing protein–protein and/or protein–carbohydrate interactions in the extra-cellular as well as intracellular milieu and regulate diverse signaling pathways, a number of which appear directed towards epithelial–mesenchymal transition and cancer stemness. Self-renewal, differentiation, long-term culturing and drug-resistance potential characterize cancer stem cells (CSCs), a small cell subpopulation within the tumor that is thought to be accountable for heterogeneity, recurrence and metastasis of tumors. Despite the fact that association of galectin-3 to the tumor stemness phenomenon is still in its infancy, there is sufficient direct evidence of its regulatory roles in CSC-associated phenotypes and signaling pathways. In this review, we have highlighted the available data on galectin-3 regulated functions pertinent to cancer stemness and explored the opportunities of its exploitation as a CSC marker and a therapeutic target.

中文翻译:

Galectin-3与癌症干性

在过去的几十年中,galectin-3是一种碳水化合物结合蛋白,对N具有亲和力-乙酰基乳糖胺残基因其在与肿瘤进展和转移相关的过程(例如细胞增殖,同型/异型聚集,动态细胞转化,迁移和侵袭,存活和凋亡)中发挥的调节作用而具有独特性。galectin-3的结构-功能关联表明,它由一个短的氨基末端基序组成,可调节其核质穿梭。胶原α样结构域,易于被基质金属蛋白酶和前列腺特异性抗原切割;负责其低聚和晶格形成,以及包含Bcl2蛋白家族抗死亡基序的碳水化合物识别/结合结构域。环境和调节多种信号传导途径,其中许多似乎是针对上皮-间质转化和癌症干性的。自我更新,分化,长期培养和耐药性是癌症干细胞(CSCs)的特征,癌症干细胞是肿瘤内的一个小细胞亚群,被认为是肿瘤的异质性,复发和转移的原因。尽管事实证明,galectin-3与肿瘤干现象的关系仍处于起步阶段,但有充分的直接证据表明其在CSC相关表型和信号通路中的调节作用。在这篇综述中,我们重点介绍了与癌干相关的半乳糖凝集素3调控功能的可用数据,并探讨了将其用作CSC标记物和治疗靶标的机会。
更新日期:2018-01-05
down
wechat
bug