YB-1 Targeted by miR-509-3-5p Affects Migration and Invasion of Triple‑Negative Breast Cancer by Regulating Cellular Epithelial‑Mesenchymal Transition.

IF 2.4 4区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Biotechnology Pub Date : 2025-03-01 Epub Date: 2024-03-04 DOI:10.1007/s12033-024-01101-0

Hanzhi Dong, Zhiqiang Peng, Tenghua Yu, Jianping Xiong

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Abstract

The epithelial-mesenchymal transition (EMT) process is closely linked to metastasis of breast cancer. This article elucidates the role of Y-box binding protein-1 (YB-1) on the migration and invasion of triple-negative breast cancer (TNBC) cells by regulating EMT, and the related mechanism. The expression data of YB-1 and miR-509-3-5p in TNBC samples and normal samples were downloaded from the GEO database. The proliferation, migration, invasion, and EMT of TNBC cells were detected by CCK-8 assay, colony formation assay, wound-healing assay, transwell assay, and immunoblotting analyses. The targeted binding of YB-1 and miR-509-3-5p was validated by luciferase reporter experiment. A xenograft mouse model was constructed to investigate the influence of the miR-509-3-5p/YB-1 axis on TNBC tumor growth in vivo. YB-1 was overexpressed, while miR-509-3-5p was underexpressed in TNBC tumor tissues and various cell lines. Silencing YB-1 depressed cell viability, proliferation, motility, and EMT in vitro, and miR-509-3-5p upregulation exerted the same effects. YB-1 was targeted by miR-509-3-5p. The suppressive effects on the phenotypes of TNBC cells caused by overexpressed miR-509-3-5p were attenuated by YB-1 upregulation. In addition, miR-509-3-5p overexpression restrained TNBC tumor growth and downregulated the YB-1-mediated EMT process in vivo. YB-1 targeted by miR-509-3-5p affects motility of TNBC cells by regulating cellular EMT.

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miR-509-3-5p 靶向的 YB-1 通过调控细胞上皮-间质转化影响三阴性乳腺癌的迁移和侵袭

上皮-间质转化（EMT）过程与乳腺癌的转移密切相关。本文阐明了Y-盒结合蛋白-1（YB-1）通过调控EMT对三阴性乳腺癌（TNBC）细胞迁移和侵袭的作用及其相关机制。从GEO数据库下载了YB-1和miR-509-3-5p在TNBC样本和正常样本中的表达数据。通过CCK-8试验、集落形成试验、伤口愈合试验、Transwell试验和免疫印迹分析检测了TNBC细胞的增殖、迁移、侵袭和EMT。荧光素酶报告实验验证了 YB-1 和 miR-509-3-5p 的靶向结合。为了研究 miR-509-3-5p/YB-1 轴对 TNBC 肿瘤体内生长的影响，我们构建了异种移植小鼠模型。在 TNBC 肿瘤组织和各种细胞系中，YB-1 过表达，而 miR-509-3-5p 低表达。沉默YB-1会抑制体外细胞活力、增殖、运动和EMT，而上调miR-509-3-5p也会产生同样的效果。miR-509-3-5p靶向YB-1。YB-1的上调减弱了过表达的miR-509-3-5p对TNBC细胞表型的抑制作用。此外，miR-509-3-5p 的过表达抑制了 TNBC 肿瘤的生长，并下调了 YB-1 介导的体内 EMT 过程。miR-509-3-5p靶向的YB-1通过调节细胞EMT影响TNBC细胞的运动性。

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

Molecular Biotechnology 医学-生化与分子生物学

CiteScore

4.10

自引率

3.80%

发文量

165

审稿时长

6 months

期刊介绍： Molecular Biotechnology publishes original research papers on the application of molecular biology to both basic and applied research in the field of biotechnology. Particular areas of interest include the following: stability and expression of cloned gene products, cell transformation, gene cloning systems and the production of recombinant proteins, protein purification and analysis, transgenic species, developmental biology, mutation analysis, the applications of DNA fingerprinting, RNA interference, and PCR technology, microarray technology, proteomics, mass spectrometry, bioinformatics, plant molecular biology, microbial genetics, gene probes and the diagnosis of disease, pharmaceutical and health care products, therapeutic agents, vaccines, gene targeting, gene therapy, stem cell technology and tissue engineering, antisense technology, protein engineering and enzyme technology, monoclonal antibodies, glycobiology and glycomics, and agricultural biotechnology.