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胃癌细胞来源的外泌体 miR-541-5p 通过 DUSP3/JAK2/STAT3 通路诱导 M2 巨噬细胞极化。

Gastric cancer cell-derived exosomal miR-541-5p induces M2 macrophage polarization through DUSP3/JAK2/STAT3 pathway.

机构信息

Department 1 of General Surgery, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi, 710068, China.

Department of Thoracic Surgery, Shaanxi Provincial People's Hospital, No. 256, West Youyi Road, Beilin District, Xi'an, Shaanxi, 710068, China.

出版信息

BMC Cancer. 2024 Aug 6;24(1):957. doi: 10.1186/s12885-024-12672-1.

DOI:10.1186/s12885-024-12672-1
PMID:39103776
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11302208/
Abstract

PURPOSE: Exosomal microRNAs have been identified as important mediators of communication between tumor cells and macrophages in the microenvironment. miR-541-5p was reported to be involved in hepatocellular carcinoma progression, but its role in gastric cancer (GC) and in GC cell-macrophage crosstalk is unknown. METHODS: Cell proliferation, migration and invasion were respectively assessed by CCK-8 assay, scratch and Transwell assays. RT-qPCR was used to detect the level of miR-541-5p, macrophage markers and DUSP3. The percentage of CD11bCD206 cell population was analyzed by flow cytometry. Western blotting was employed to evaluate DUSP3-JAK2/STAT3 pathway proteins and exosome markers. The interaction between miR-541-5p and DUSP3 was verified by luciferase assay. RESULTS: The results showed that miR-541-5p was upregulated in GC tissues and cells, and stimulated GC cell growth, migration and invasion in vitro. GC cells induce M2 macrophage polarization by secreting the exosomal miR-541-5p. Exosomal miR-541-5p maintained JAK2/STAT3 pathway activation in macrophages by targeting negative regulation of DUSP3. Inhibiting miR-541-5p significantly limited tumor growth in vivo. CONCLUSION: In conclusion, miR-541-5p promotes GC cell progression. GC cells may induce macrophage M2 polarization through the exosomal miR-541-5p-mediated DUSP3/JAK2/STAT3 pathway. miR-541-5p may be a potential therapeutic target for GC.

摘要

目的：外泌体 microRNAs 已被鉴定为肿瘤细胞与微环境中巨噬细胞之间通讯的重要介质。miR-541-5p 被报道参与肝细胞癌的进展，但它在胃癌（GC）中的作用及其在 GC 细胞-巨噬细胞串扰中的作用尚不清楚。

方法：通过 CCK-8 测定、划痕和 Transwell 测定分别评估细胞增殖、迁移和侵袭。使用 RT-qPCR 检测 miR-541-5p、巨噬细胞标志物和 DUSP3 的水平。通过流式细胞术分析 CD11bCD206 细胞群的百分比。采用 Western blot 评估 DUSP3-JAK2/STAT3 通路蛋白和外泌体标志物。通过荧光素酶测定验证 miR-541-5p 和 DUSP3 之间的相互作用。

结果：结果表明，miR-541-5p 在 GC 组织和细胞中上调，并在体外刺激 GC 细胞的生长、迁移和侵袭。GC 细胞通过分泌外泌体 miR-541-5p 诱导 M2 巨噬细胞极化。外泌体 miR-541-5p 通过靶向 DUSP3 的负调控来维持巨噬细胞中 JAK2/STAT3 通路的激活。抑制 miR-541-5p 显著限制了体内肿瘤的生长。

结论：总之，miR-541-5p 促进 GC 细胞的进展。GC 细胞可能通过外泌体 miR-541-5p 介导的 DUSP3/JAK2/STAT3 通路诱导巨噬细胞 M2 极化。miR-541-5p 可能是 GC 的一个潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/6b648609d321/12885_2024_12672_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/5e6f6b8e092b/12885_2024_12672_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/32c1a42861b5/12885_2024_12672_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/7f3539fac920/12885_2024_12672_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/9cbcee800dd5/12885_2024_12672_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/370406667105/12885_2024_12672_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/6b648609d321/12885_2024_12672_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/5e6f6b8e092b/12885_2024_12672_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/32c1a42861b5/12885_2024_12672_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/7f3539fac920/12885_2024_12672_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/9cbcee800dd5/12885_2024_12672_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/370406667105/12885_2024_12672_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/68a4/11302208/6b648609d321/12885_2024_12672_Fig6_HTML.jpg

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引用本文的文献

[1]
Recent progress in the study of exosomes in the gastric cancer immune microenvironment.

Front Immunol. 2025-7-23

[2]
Targeting tumor-associated macrophages in gastric cancer progression and therapy: insights from molecular mechanisms to therapeutic applications.

Front Pharmacol. 2025-6-17

[3]
Tumor-derived vesicles in immune modulation: focus on signaling pathways.

Front Immunol. 2025-5-15

[4]
Functions and Clinical Applications of Exosomes in Gastric Cancer.

Int J Biol Sci. 2025-2-28

[5]
Tumour-derived exosomal miR-205 promotes ovarian cancer cell progression through M2 macrophage polarization via the PI3K/Akt/mTOR pathway.

J Ovarian Res. 2025-2-15

[6]
Gastric cancer-derived exosomal let-7 g-5p mediated by SERPINE1 promotes macrophage M2 polarization and gastric cancer progression.

J Exp Clin Cancer Res. 2025-1-2

本文引用的文献

[1]
JAK-STAT Signaling in Inflammatory Breast Cancer Enables Chemotherapy-Resistant Cell States.

Cancer Res. 2023-1-18

[2]
Hydroxyzine Induces Cell Death in Triple-Negative Breast Cancer Cells via Mitochondrial Superoxide and Modulation of Jak2/STAT3 Signaling.

Biomol Ther (Seoul). 2022-11-1

[3]
JAK2/STAT3 Axis Intermediates Microglia/Macrophage Polarization During Cerebral Ischemia/Reperfusion Injury.

Neuroscience. 2022-8-1

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CircPCBP2 promotes the stemness and chemoresistance of DLBCL via targeting miR-33a/b to disinhibit PD-L1.

Cancer Sci. 2022-8

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CircRTN4IP1 regulates the malignant progression of intrahepatic cholangiocarcinoma by sponging miR-541-5p to induce HIF1A production.

Pathol Res Pract. 2022-2

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Cucurbitacin B controls M2 macrophage polarization to suppresses metastasis via targeting JAK-2/STAT3 signalling pathway in colorectal cancer.

J Ethnopharmacol. 2022-4-6

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CircMTO1 suppresses hepatocellular carcinoma progression via the miR-541-5p/ZIC1 axis by regulating Wnt/β-catenin signaling pathway and epithelial-to-mesenchymal transition.

Cell Death Dis. 2021-12-20

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Mol Ther. 2022-3-2

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Exosomal miR-1246 from glioma patient body fluids drives the differentiation and activation of myeloid-derived suppressor cells.

Mol Ther. 2021-12-1

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J Hum Genet. 2021-9

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