NEAT1 promotes the progression of prostate cancer by targeting the miR-582-5p/EZH2 regulatory axis

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS

ACS Applied Bio Materials Pub Date : 2024-02-14 DOI:10.1007/s10616-023-00612-z

Weiqiang Xu, Yu Wu, Guoxi Zhang

{"title":"NEAT1 promotes the progression of prostate cancer by targeting the miR-582-5p/EZH2 regulatory axis","authors":"Weiqiang Xu, Yu Wu, Guoxi Zhang","doi":"10.1007/s10616-023-00612-z","DOIUrl":null,"url":null,"abstract":"<h3>Abstract</h3> <p>In several forms of malignant tumors, nuclear enriched abundant transcript 1 (NEAT1), a lncRNA, has been identified to play an important role. NEAT1’s regulation patterns in prostate cancer (PCa) are, however, mainly unknown. This study was aimed to evaluate and study the roles and regulatory mechanisms of NEAT1 in PCa. NEAT1, miR-582-5p, and enhancer of zeste homolog 2 (EZH2) expression were detected by qRT-PCR. The PCa cells’ invasive, migrative, and proliferative activities in vitro were assessed using transwell migration and invasion, wound-healing, cloning creation, and CCK-8 assays. In the present study, impaired proliferative, migrative, and invasive capacities were observed in the NEAT1-deficient PCa (PC3 and LNCaP) cells. Further mechanistic studies found that NEAT1 performs its function through sponging miR-582-5p. Furthermore, EZH2 was confirmed to be the downstream target gene of miRNA-582-5p. The impaired progression caused by NEAT1 deficiency in PCa cells was significantly restored by the inhibition of miR-582-5p, while these effects were largely abolished by the deletion of EZH2. Finally, the xenograft nude mouse model showed that knocking down the expression of NEAT1 suppressed the growth of PCa. In conclusion, NEAT1 promotes the progression of PCa by controlling the miR-582-5p and miR-582-5p-mediated EZH2.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s10616-023-00612-z","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}

引用次数: 0

Abstract

In several forms of malignant tumors, nuclear enriched abundant transcript 1 (NEAT1), a lncRNA, has been identified to play an important role. NEAT1’s regulation patterns in prostate cancer (PCa) are, however, mainly unknown. This study was aimed to evaluate and study the roles and regulatory mechanisms of NEAT1 in PCa. NEAT1, miR-582-5p, and enhancer of zeste homolog 2 (EZH2) expression were detected by qRT-PCR. The PCa cells’ invasive, migrative, and proliferative activities in vitro were assessed using transwell migration and invasion, wound-healing, cloning creation, and CCK-8 assays. In the present study, impaired proliferative, migrative, and invasive capacities were observed in the NEAT1-deficient PCa (PC3 and LNCaP) cells. Further mechanistic studies found that NEAT1 performs its function through sponging miR-582-5p. Furthermore, EZH2 was confirmed to be the downstream target gene of miRNA-582-5p. The impaired progression caused by NEAT1 deficiency in PCa cells was significantly restored by the inhibition of miR-582-5p, while these effects were largely abolished by the deletion of EZH2. Finally, the xenograft nude mouse model showed that knocking down the expression of NEAT1 suppressed the growth of PCa. In conclusion, NEAT1 promotes the progression of PCa by controlling the miR-582-5p and miR-582-5p-mediated EZH2.

Abstract Image

查看原文本刊更多论文

NEAT1 通过靶向 miR-582-5p/EZH2 调控轴促进前列腺癌的进展

摘要在多种形式的恶性肿瘤中，核富集丰富转录本1（NEAT1）（一种lncRNA）被认为发挥着重要作用。然而，NEAT1在前列腺癌（PCa）中的调控模式尚不清楚。本研究旨在评估和研究 NEAT1 在 PCa 中的作用和调控机制。研究采用 qRT-PCR 技术检测了 NEAT1、miR-582-5p 和泽斯特同源增强子 2（EZH2）的表达。使用transwell迁移和侵袭、伤口愈合、克隆创建和CCK-8试验评估了PCa细胞在体外的侵袭、迁移和增殖活性。在本研究中，观察到 NEAT1 缺失的 PCa（PC3 和 LNCaP）细胞增殖、迁移和侵袭能力受损。进一步的机理研究发现，NEAT1 通过疏导 miR-582-5p 发挥其功能。此外，EZH2 被证实是 miRNA-582-5p 的下游靶基因。通过抑制 miR-582-5p，PCa 细胞因 NEAT1 缺乏而导致的进展受阻得到了明显的恢复，而通过删除 EZH2，这些影响基本消失。最后，异种移植裸鼠模型显示，敲除 NEAT1 的表达可抑制 PCa 的生长。总之，NEAT1通过控制miR-582-5p和miR-582-5p介导的EZH2来促进PCa的进展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464