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文章:

自噬在癌症进展过程中对上皮间质转化诱导的贡献

Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression

原文发布日期:16 February 2024

DOI: 10.3390/cancers16040807

类型: Article

开放获取: 是

 

英文摘要:

Epithelial Mesenchymal Transition (EMT) is a dedifferentiation process implicated in many physio-pathological conditions including tumor transformation. EMT is regulated by several extracellular mediators and under certain conditions it can be reversible. Autophagy is a conserved catabolic process in which intracellular components such as protein/DNA aggregates and abnormal organelles are degraded in specific lysosomes. In cancer, autophagy plays a controversial role, acting in different conditions as both a tumor suppressor and a tumor-promoting mechanism. Experimental evidence shows that deep interrelations exist between EMT and autophagy-related pathways. Although this interplay has already been analyzed in previous studies, understanding mechanisms and the translational implications of autophagy/EMT need further study. The role of autophagy in EMT is not limited to morphological changes, but activation of autophagy could be important to DNA repair/damage system, cell adhesion molecules, and cell proliferation and differentiation processes. Based on this, both autophagy and EMT and related pathways are now considered as targets for cancer therapy. In this review article, the contribution of autophagy to EMT and progression of cancer is discussed. This article also describes the multiple connections between EMT and autophagy and their implication in cancer treatment.

 

摘要翻译: 

上皮间质转化(EMT)是一种涉及多种生理病理状态(包括肿瘤转化)的去分化过程。该过程受多种细胞外介质调控,并在特定条件下具有可逆性。自噬是一种保守的分解代谢过程,其中蛋白质/DNA聚集体及异常细胞器等细胞内成分在特定溶酶体中被降解。在癌症中,自噬扮演着矛盾的双重角色:在不同条件下既可抑制肿瘤发展,亦可促进肿瘤进展。实验证据表明EMT与自噬相关通路存在深度关联。尽管既往研究已对此相互作用进行探讨,但对自噬/EMT作用机制及其转化医学意义仍需深入研究。自噬在EMT中的作用不仅限于形态学改变,其激活对DNA修复/损伤系统、细胞黏附分子以及细胞增殖分化过程均具有重要意义。基于此,自噬与EMT及其相关通路现已成为癌症治疗的潜在靶点。本文综述了自噬对EMT及癌症进展的影响机制,系统阐述了EMT与自噬的多重关联及其在癌症治疗中的意义。

 

原文链接:

Contribution of Autophagy to Epithelial Mesenchymal Transition Induction during Cancer Progression

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