Long non-coding RNA PRSS23-AS1 as ceRNA promotes breast cancer progression by regulating EMT via miR-3176 /YBX1 axis.

IF 4.8 3区医学 Q1 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Cancer gene therapy Pub Date : 2025-07-24 DOI:10.1038/s41417-025-00943-3

Yun Huang, Mudan Feng, Yiwei Jiang, Maihuan Wang, Mingkun Wang, Zhen Cao

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引用次数: 0

Abstract

Breast cancer (BC) remains a leading cause of cancer-related mortality, largely due to its aggressive proliferation and metastatic potential. Long non-coding RNAs (lncRNAs) have emerged as key regulators in tumor development and progression. This study explored the functional role and mechanism of Lnc-PRSS23-AS1 in BC. We assessed Lnc-PRSS23-AS1 expression and localization using fluorescence in situ hybridization, qRT-PCR, and Western blotting in BC tissues and cell lines. Binding interactions between Lnc-PRSS23-AS1, miR-3176, and Y-box binding protein 1 (YBX1) were validated through dual-luciferase reporter assays, RNA pulldown, and RNA immunoprecipitation. Lnc-PRSS23-AS1 was significantly upregulated in BC and predominantly localized in the cytoplasm. Silencing Lnc-PRSS23-AS1 or overexpressing miR-3176 suppressed BC cell proliferation, migration, and invasion in vitro and in vivo. Conversely, miR-3176 inhibition or YBX1 overexpression reversed these effects. Mechanistically, Lnc-PRSS23-AS1 promoted YBX1 protein expression by acting as a molecular sponge for miR-3176. These findings highlight the Lnc-PRSS23-AS1/miR-3176/YBX1 axis as a driver of BC progression and suggest Lnc-PRSS23-AS1 as a potential therapeutic target for breast cancer treatment.

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长链非编码RNA PRSS23-AS1作为ceRNA通过miR-3176 /YBX1轴调控EMT促进乳腺癌进展。

乳腺癌（BC）仍然是癌症相关死亡的主要原因，主要是由于其侵袭性增殖和转移潜力。长链非编码rna （lncRNAs）已成为肿瘤发生和发展的关键调控因子。本研究探讨Lnc-PRSS23-AS1在BC中的功能作用及机制。我们使用荧光原位杂交、qRT-PCR和Western blotting技术评估了Lnc-PRSS23-AS1在BC组织和细胞系中的表达和定位。Lnc-PRSS23-AS1、miR-3176和Y-box结合蛋白1 （YBX1）之间的结合相互作用通过双荧光素酶报告基因检测、RNA下拉和RNA免疫沉淀验证。Lnc-PRSS23-AS1在BC中显著上调，且主要定位于细胞质中。在体外和体内，沉默Lnc-PRSS23-AS1或过表达miR-3176抑制BC细胞的增殖、迁移和侵袭。相反，miR-3176抑制或YBX1过表达逆转了这些作用。在机制上，Lnc-PRSS23-AS1通过作为miR-3176的分子海绵促进YBX1蛋白的表达。这些发现强调了Lnc-PRSS23-AS1/miR-3176/YBX1轴是BC进展的驱动因素，并提示Lnc-PRSS23-AS1是乳腺癌治疗的潜在治疗靶点。

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

Cancer gene therapy 医学-生物工程与应用微生物

CiteScore

10.20

自引率

0.00%

发文量

150

审稿时长

4-8 weeks

期刊介绍： Cancer Gene Therapy is the essential gene and cellular therapy resource for cancer researchers and clinicians, keeping readers up to date with the latest developments in gene and cellular therapies for cancer. The journal publishes original laboratory and clinical research papers, case reports and review articles. Publication topics include RNAi approaches, drug resistance, hematopoietic progenitor cell gene transfer, cancer stem cells, cellular therapies, homologous recombination, ribozyme technology, antisense technology, tumor immunotherapy and tumor suppressors, translational research, cancer therapy, gene delivery systems (viral and non-viral), anti-gene therapy (antisense, siRNA & ribozymes), apoptosis; mechanisms and therapies, vaccine development, immunology and immunotherapy, DNA synthesis and repair. Cancer Gene Therapy publishes the results of laboratory investigations, preclinical studies, and clinical trials in the field of gene transfer/gene therapy and cellular therapies as applied to cancer research. Types of articles published include original research articles; case reports; brief communications; review articles in the main fields of drug resistance/sensitivity, gene therapy, cellular therapy, tumor suppressor and anti-oncogene therapy, cytokine/tumor immunotherapy, etc.; industry perspectives; and letters to the editor.