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癌症中的糖基化:多药耐药性与上皮-间质转化之间的相互作用?

Glycosylation in Cancer: Interplay between Multidrug Resistance and Epithelial-to-Mesenchymal Transition?

作者信息

da Fonseca Leonardo Marques, da Silva Vanessa Amil, Freire-de-Lima Leonardo, Previato José Osvaldo, Mendonça-Previato Lucia, Capella Márcia Alves Marques

机构信息

Laboratório de Glicobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro , Rio de Janeiro, Rio de Janeiro , Brazil.

Laboratório de Glicobiologia, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil; Laboratório de P&D em Práticas Integrativas e Complementares, Faculdade de Farmácia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil.

出版信息

Front Oncol. 2016 Jun 22;6:158. doi: 10.3389/fonc.2016.00158. eCollection 2016.

DOI:10.3389/fonc.2016.00158
PMID:27446804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4916178/
Abstract

The expression of unusual glycan structures is a hallmark of cancer progression, and their functional roles in cancer biology have been extensively investigated in epithelial-to-mesenchymal transition (EMT) models. EMT is a physiological process involved in embryonic development and wound healing. It is characterized by loss of epithelial cell polarity and cell adhesion, permitting cell migration, and thus formation of new epithelia. However, this process is unwanted when occurring outside their physiological limit, resulting in fibrosis of organs and progression of cancer and metastasis. Several studies observed that EMT is related to the acquisition of multidrug resistance (MDR) phenotype, a condition in which cancer cells acquire resistance to multiple different drugs, which has virtually nothing in common. However, although some studies suggested interplay between these two apparently distinct phenomena, almost nothing is known about this possible relationship. A common pathway to them is the need for glycosylation, a post-translational modification that can alter biological function. Thus, this review intends to compile the main facts obtained until now in these two areas, as an effort to unravel the relationship between EMT and MDR.

摘要

异常聚糖结构的表达是癌症进展的一个标志,并且它们在癌症生物学中的功能作用已在上皮-间质转化(EMT)模型中得到广泛研究。EMT是一个参与胚胎发育和伤口愈合的生理过程。其特征是上皮细胞极性和细胞黏附丧失,使细胞能够迁移,从而形成新的上皮组织。然而,当这个过程在其生理极限之外发生时是有害的,会导致器官纤维化以及癌症进展和转移。多项研究观察到EMT与多药耐药(MDR)表型的获得有关,在这种情况下癌细胞对多种不同药物产生耐药性,而这些药物几乎没有共同之处。然而,尽管一些研究表明这两种明显不同的现象之间存在相互作用,但对于这种可能的关系几乎一无所知。它们的一个共同途径是对糖基化的需求,糖基化是一种可以改变生物学功能的翻译后修饰。因此,本综述旨在汇总迄今为止在这两个领域获得的主要事实,以努力阐明EMT与MDR之间的关系。

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