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结直肠癌细胞来源的细胞外囊泡通过 NOD1 信号通路促进转移。

Extracellular vesicles from colorectal cancer cells promote metastasis via the NOD1 signalling pathway.

机构信息

School of Pharmaceutical Sciences, Tsinghua University, Beijing, P. R. China.

Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, P. R. China.

出版信息

J Extracell Vesicles. 2022 Sep;11(9):e12264. doi: 10.1002/jev2.12264.

DOI:10.1002/jev2.12264
PMID:36068649
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9448875/
Abstract

Pattern-recognition receptors (PRRs) have been shown to promote tumour metastasis via sensing tumour cell-derived small extracellular vesicles (EVs). Nucleotide-binding oligomerisation domain 1 (NOD1), a cytoplasmic PRR, plays a role in colorectal cancer (CRC) by detecting bacterial products. However, the precise mechanisms underlying the effects of NOD1, following identification of CRC cell-derived EVs (CRC-EVs), to potentiate CRC liver metastasis (CRC-LM), remain poorly understood. Here, we demonstrate that CRC-EVs activate NOD1 in macrophages to initiate secretion of inflammatory cytokines and chemokines. NOD1-activated macrophages also promote CRC cell migration, while in a murine model of liver metastasis (LM), NOD1-deficient mice exhibit reduced metastasis following CRC-EV treatment. Furthermore, cell division cycle 42 (CDC42), a small Rho guanosine-5'-triphosphate (GTP)ase, is delivered by CRC-EVs into macrophages where it activates NOD1. In addition, EVs from the plasma of patients with CRC-LM mediate NOD1 activation in human peripheral blood mononuclear cells. Moreover, high NOD1 expression in tumour tissues is associated with poor prognosis of CRC-LM. Our findings suggest that CRC-EVs activate NOD1 to promote tumour metastasis, thus, NOD1 may serve as a potential target in the diagnosis and treatment of CRC-LM.

摘要

模式识别受体 (PRRs) 通过感知肿瘤细胞衍生的小细胞外囊泡 (EVs) 促进肿瘤转移。核苷酸结合寡聚化结构域 1 (NOD1) 是一种细胞质 PRR，通过检测细菌产物在结直肠癌 (CRC) 中发挥作用。然而，在鉴定 CRC 细胞衍生的 EV (CRC-EVs) 后，NOD1 促进 CRC 肝转移 (CRC-LM) 的精确机制仍知之甚少。在这里，我们证明 CRC-EVs 在巨噬细胞中激活 NOD1 以启动炎症细胞因子和趋化因子的分泌。NOD1 激活的巨噬细胞还促进 CRC 细胞迁移，而在肝转移 (LM) 的小鼠模型中，NOD1 缺陷小鼠在接受 CRC-EV 治疗后转移减少。此外，细胞分裂周期蛋白 42 (CDC42)，一种小的 Rho 鸟苷酸-5'-三磷酸 (GTP) 酶，被 CRC-EVs 递送到巨噬细胞中，在那里它激活 NOD1。此外，来自 CRC-LM 患者血浆的 EV 在人外周血单核细胞中介导 NOD1 激活。此外，肿瘤组织中 NOD1 的高表达与 CRC-LM 的预后不良相关。我们的研究结果表明，CRC-EVs 通过激活 NOD1 促进肿瘤转移，因此，NOD1 可能是 CRC-LM 诊断和治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/0821b1bbc426/JEV2-11-e12264-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/2b352f69d300/JEV2-11-e12264-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/1b0f045437ef/JEV2-11-e12264-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/faa37c1052a6/JEV2-11-e12264-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/966c6266612b/JEV2-11-e12264-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/0235588daf62/JEV2-11-e12264-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/98a8e0114dcb/JEV2-11-e12264-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/0821b1bbc426/JEV2-11-e12264-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/2b352f69d300/JEV2-11-e12264-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/1b0f045437ef/JEV2-11-e12264-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/faa37c1052a6/JEV2-11-e12264-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/966c6266612b/JEV2-11-e12264-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/0235588daf62/JEV2-11-e12264-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/98a8e0114dcb/JEV2-11-e12264-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/40b1/9448875/0821b1bbc426/JEV2-11-e12264-g004.jpg

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