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反式高尔基体网络与肿瘤进展之间的联系。

The link between the trans-Golgi network and tumour progression.

作者信息

Jahangiri Leila

机构信息

School of Science and Technology, Nottingham Trent University, Clifton Site, Nottingham, NG11 8NS, UK.

Division of Cellular and Molecular Pathology, Department of Pathology, Addenbrookes Hospital, University of Cambridge, Cambridge, CB0 2QQ, UK.

出版信息

Mol Biol Rep. 2025 Apr 28;52(1):435. doi: 10.1007/s11033-025-10548-6.

DOI:10.1007/s11033-025-10548-6
PMID:40293576
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12037649/
Abstract

The trans-Golgi network is a major sorting organelle consisting of a tubular membrane originating from the trans-Golgi cisternae. Proteins and lipids synthesised in the endoplasmic reticulum are transported through the Golgi apparatus and sorted in the trans-Golgi network into pleomorphic transport carriers targeted for various destinations. These destinations include the apical and basolateral membranes, early and late, recycling endosomes, and secretory granules. The trans-Golgi network also accepts retrograde endosome traffic, contributing to the recycling of proteins and lipids, and, therefore, sits at the crossroads of secretory and endosomal systems. Cancer is a somatic evolutionary process that comprises the accumulation of mutations that contribute to tumourigenesis, growth, progression, immune evasion, and resistance to therapy. This study aims to catalogue how multiple components and players of the trans-Golgi network affect tumour progression. Further, the link between the tumour microenvironment, the trans-Golgi network, and tumour progression will be dissected. A more profound understanding of these mechanisms will inform better treatment options.

摘要

反式高尔基体网络是一种主要的分拣细胞器,由源自反式高尔基体潴泡的管状膜组成。在内质网中合成的蛋白质和脂质通过高尔基体运输,并在反式高尔基体网络中被分拣到靶向不同目的地的多形性运输载体中。这些目的地包括顶端和基底外侧膜、早期和晚期再循环内体以及分泌颗粒。反式高尔基体网络还接受逆行性内体运输,促进蛋白质和脂质的再循环,因此处于分泌系统和内体系统的交叉点。癌症是一个体细胞进化过程,包括导致肿瘤发生、生长、进展、免疫逃逸和治疗抗性的突变积累。本研究旨在编目反式高尔基体网络的多个组成部分和参与者如何影响肿瘤进展。此外,将剖析肿瘤微环境、反式高尔基体网络与肿瘤进展之间的联系。对这些机制更深入的理解将为更好的治疗选择提供依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/e5fec8d87fbc/11033_2025_10548_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/9084c14ca80a/11033_2025_10548_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/ac02c1b248ae/11033_2025_10548_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/5191135ab5d3/11033_2025_10548_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/cbd59e70fde3/11033_2025_10548_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/e5fec8d87fbc/11033_2025_10548_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/9084c14ca80a/11033_2025_10548_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/ac02c1b248ae/11033_2025_10548_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/5191135ab5d3/11033_2025_10548_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/cbd59e70fde3/11033_2025_10548_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4823/12037649/e5fec8d87fbc/11033_2025_10548_Fig5_HTML.jpg

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本文引用的文献

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Targeting the ERK1/2 and p38 MAPK pathways attenuates Golgi tethering factor golgin-97 depletion-induced cancer progression in breast cancer.靶向ERK1/2和p38丝裂原活化蛋白激酶(MAPK)信号通路可减轻高尔基体拴系因子高尔基体蛋白97缺失诱导的乳腺癌进展。
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GCC2 promotes non-small cell lung cancer progression by maintaining Golgi apparatus integrity and stimulating EGFR signaling pathways.GCC2 通过维持高尔基体的完整性和刺激 EGFR 信号通路促进非小细胞肺癌的进展。
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RAB42 overexpression correlates with poor prognosis, immune cell infiltration and chemoresistance.
RAB42过表达与不良预后、免疫细胞浸润和化疗耐药相关。
Front Pharmacol. 2024 Jul 19;15:1445170. doi: 10.3389/fphar.2024.1445170. eCollection 2024.
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Syntaxin6 contributes to hepatocellular carcinoma tumorigenesis via enhancing STAT3 phosphorylation.Syntaxin6通过增强STAT3磷酸化促进肝细胞癌的肿瘤发生。
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