关键词: Cancer EMT Epithelial-mesenchymal plasticity Fibrosis Galectin Metastasis Tissue repair

Mesh : Humans Galectins / genetics metabolism Fibrosis Glycoproteins Epithelial-Mesenchymal Transition Glycolipids Neoplasms

来  源:   DOI:10.1186/s40659-024-00490-5   PDF(Pubmed)

Abstract:
Galectins are soluble glycan-binding proteins that interact with a wide range of glycoproteins and glycolipids and modulate a broad spectrum of physiological and pathological processes. The expression and subcellular localization of different galectins vary among tissues and cell types and change during processes of tissue repair, fibrosis and cancer where epithelial cells loss differentiation while acquiring migratory mesenchymal phenotypes. The epithelial-mesenchymal transition (EMT) that occurs in the context of these processes can include modifications of glycosylation patterns of glycolipids and glycoproteins affecting their interactions with galectins. Moreover, overexpression of certain galectins has been involved in the development and different outcomes of EMT. This review focuses on the roles and mechanisms of Galectin-1 (Gal-1), Gal-3, Gal-4, Gal-7 and Gal-8, which have been involved in physiologic and pathogenic EMT contexts.
摘要:
半乳糖凝集素是可溶性聚糖结合蛋白,其与宽范围的糖蛋白和糖脂相互作用并调节广谱的生理和病理过程。不同半乳糖凝集素的表达和亚细胞定位在不同组织和细胞类型之间存在差异,并在组织修复过程中发生变化。纤维化和癌症,其中上皮细胞失去分化,同时获得迁移间充质表型。在这些过程的背景下发生的上皮-间质转化(EMT)可以包括糖脂和糖蛋白的糖基化模式的修饰,影响它们与半乳糖凝集素的相互作用。此外,某些半乳糖凝集素的过表达已参与EMT的发展和不同结果。本文就半乳糖凝集素-1(Gal-1)的作用及作用机制进行综述,Gal-3,Gal-4,Gal-7和Gal-8,已参与生理和致病性EMT背景。
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