Exploring Retrograde Trafficking: Mechanisms and Consequences in Cancer and Disease.

IF 3.6 3区生物学 Q3 CELL BIOLOGY

Traffic Pub Date : 2024-02-01 DOI:10.1111/tra.12931

Rachel Bingham, Helen McCarthy, Niamh Buckley

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引用次数: 0

Abstract

Retrograde trafficking (RT) orchestrates the intracellular movement of cargo from the plasma membrane, endosomes, Golgi or endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC) in an inward/ER-directed manner. RT works as the opposing movement to anterograde trafficking (outward secretion), and the two work together to maintain cellular homeostasis. This is achieved through maintaining cell polarity, retrieving proteins responsible for anterograde trafficking and redirecting proteins that become mis-localised. However, aberrant RT can alter the correct location of key proteins, and thus inhibit or indeed change their canonical function, potentially causing disease. This review highlights the recent advances in the understanding of how upregulation, downregulation or hijacking of RT impacts the localisation of key proteins in cancer and disease to drive progression. Cargoes impacted by aberrant RT are varied amongst maladies including neurodegenerative diseases, autoimmune diseases, bacterial and viral infections (including SARS-CoV-2), and cancer. As we explore the intricacies of RT, it becomes increasingly apparent that it holds significant potential as a target for future therapies to offer more effective interventions in a wide range of pathological conditions.

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探索逆向贩运：癌症和疾病的机制与后果》。

逆行运输（RT）以内向/外向的方式协调来自质膜、内体、高尔基体或内质网（ER）-高尔基体中间区室（ERGIC）的货物在细胞内的移动。RT是逆向运输（向外分泌）的对立运动，两者共同作用以维持细胞平衡。这是通过维持细胞极性、检索负责逆向运输的蛋白质以及重新定向定位错误的蛋白质来实现的。然而，异常 RT 会改变关键蛋白的正确位置，从而抑制或改变它们的典型功能，可能导致疾病。本综述将重点介绍在了解 RT 的上调、下调或劫持如何影响癌症和疾病中关键蛋白的定位从而推动疾病进展方面取得的最新进展。受异常 RT 影响的货物种类繁多，包括神经退行性疾病、自身免疫性疾病、细菌和病毒感染（包括 SARS-CoV-2）以及癌症。随着我们对 RT 复杂性的探索，我们越来越清楚地认识到，RT 作为未来疗法的一个靶点具有巨大的潜力，可为各种病理状况提供更有效的干预。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Traffic 生物-细胞生物学

CiteScore

8.10

自引率

2.20%

发文量

审稿时长

2 months

期刊介绍： Traffic encourages and facilitates the publication of papers in any field relating to intracellular transport in health and disease. Traffic papers span disciplines such as developmental biology, neuroscience, innate and adaptive immunity, epithelial cell biology, intracellular pathogens and host-pathogen interactions, among others using any eukaryotic model system. Areas of particular interest include protein, nucleic acid and lipid traffic, molecular motors, intracellular pathogens, intracellular proteolysis, nuclear import and export, cytokinesis and the cell cycle, the interface between signaling and trafficking or localization, protein translocation, the cell biology of adaptive an innate immunity, organelle biogenesis, metabolism, cell polarity and organization, and organelle movement. All aspects of the structural, molecular biology, biochemistry, genetics, morphology, intracellular signaling and relationship to hereditary or infectious diseases will be covered. Manuscripts must provide a clear conceptual or mechanistic advance. The editors will reject papers that require major changes, including addition of significant experimental data or other significant revision. Traffic will consider manuscripts of any length, but encourages authors to limit their papers to 16 typeset pages or less.