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微小RNA-224通过靶向Akirin1激活癌症相关成纤维细胞，以增强肺癌细胞的迁移和侵袭能力。

miR-224 activates cancer-associated fibroblasts to enhance lung cancer cell migration and invasion by targeting Akirin1.

作者信息

Oh Seonyeong, Lee Sieun, Cheon Inyoung, Ahn Young-Ho

机构信息

Department of Molecular Medicine, Inflammation-Cancer Microenvironment Research Center, College of Medicine, Ewha Womans University, 25 Magokdong-ro 2-gil, Gangseo-gu, Seoul, 07804, Korea.

出版信息

Sci Rep. 2025 Jan 24;15(1):3050. doi: 10.1038/s41598-024-82189-x.

DOI:10.1038/s41598-024-82189-x
PMID:39856124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11760386/
Abstract

Cancer-associated fibroblasts (CAFs) actively contribute to the formation of tumor-supportive microenvironments, thereby promoting cancer progression and impacting therapeutic outcomes. This study utilized global microRNA (miRNA) expression profiling to identify specific miRNAs responsible for reprogramming normal lung fibroblasts (LFs) into CAFs. miR-224 demonstrates increased expression in CAFs, and its levels are elevated in lung tumors compared to those in normal tissues, according to data from public databases. Overexpression of miR-224 in LFs increases the overall expression of CAF activation markers. Furthermore, LFs overexpressing miR-224 enhanced the migration and invasion of lung cancer cells via direct cell-to-cell contact in a co-culture system. In a mouse orthotopic injection model, miR-224 overexpression in LFs increased lung cancer metastasis. Using target prediction tools and subsequent 3'-UTR luciferase assay, Akirin1 was validated as a direct target gene of miR-224. In addition, LFs depleted of Akirin1 by siRNAs stimulated the migration and invasion of lung cancer cells compared to control LFs. Overall, these findings indicate that miR-224 induces CAF activation and promotes the migration and invasion of lung cancer cells by targeting Akirin1 in co-culture systems.

摘要

癌症相关成纤维细胞（CAFs）积极参与肿瘤支持性微环境的形成，从而促进癌症进展并影响治疗效果。本研究利用全局微小RNA（miRNA）表达谱来鉴定负责将正常肺成纤维细胞（LFs）重编程为CAFs的特定miRNA。根据公共数据库的数据，miR-224在CAFs中的表达增加，并且其在肺肿瘤中的水平相对于正常组织升高。在LFs中过表达miR-224会增加CAF激活标志物的整体表达。此外，过表达miR-224的LFs在共培养系统中通过直接的细胞间接触增强了肺癌细胞的迁移和侵袭。在小鼠原位注射模型中，LFs中miR-224的过表达增加了肺癌转移。使用靶标预测工具和随后的3'-UTR荧光素酶测定，Akirin1被验证为miR-

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/b61fe292211f/41598_2024_82189_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/5e5c67a324e6/41598_2024_82189_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/9622dcd60f54/41598_2024_82189_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/65ee98f25161/41598_2024_82189_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/b61fe292211f/41598_2024_82189_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/5e5c67a324e6/41598_2024_82189_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/9622dcd60f54/41598_2024_82189_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/65ee98f25161/41598_2024_82189_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6344/11760386/b61fe292211f/41598_2024_82189_Fig4_HTML.jpg

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本文引用的文献

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MiR-224 promotes lymphatic metastasis by targeting ANGPTL1 in non-small-cell lung carcinoma.
miR-224 通过靶向 ANGPTL1 促进非小细胞肺癌的淋巴转移。
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MiR-224-5p Targeting OCLN Promotes the Proliferation, Migration, and Invasion of Clear Cell Renal Cell Carcinoma Cells.miR-224-5p 靶向 OCLN 促进肾透明细胞癌细胞的增殖、迁移和侵袭。
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Extracellular vesicles derived from cancer-associated fibroblast carries miR-224-5p targeting SLC4A4 to promote the proliferation, invasion and migration of colorectal cancer cells.源自癌症相关成纤维细胞的细胞外囊泡携带 miR-224-5p 靶向 SLC4A4 促进结直肠癌细胞的增殖、侵袭和迁移。
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HIF-1α is necessary for activation and tumour-promotion effect of cancer-associated fibroblasts in lung cancer.缺氧诱导因子-1α（HIF-1α）在肺癌相关成纤维细胞的激活和促肿瘤效应中是必需的。
J Cell Mol Med. 2021 Jun;25(12):5457-5469. doi: 10.1111/jcmm.16556. Epub 2021 May 4.
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