ZNF197-AS1/miR-425/GABARAPL1 Axis: A Novel Regulatory Mechanism in Uveal Melanoma.

IF 5 2区生物学 Q2 CELL BIOLOGY American journal of physiology. Cell physiology Pub Date : 2024-09-23 DOI:10.1152/ajpcell.00457.2024

Chao Zhang, Shuai Wu

{"title":"ZNF197-AS1/miR-425/GABARAPL1 Axis: A Novel Regulatory Mechanism in Uveal Melanoma.","authors":"Chao Zhang, Shuai Wu","doi":"10.1152/ajpcell.00457.2024","DOIUrl":null,"url":null,"abstract":"This study investigates the role of the long non-coding RNA (lncRNA) ZNF197-AS1 in uveal melanoma (UM), focusing on its function within a competing endogenous RNA (ceRNA) network. Utilizing the UM-related TCGA dataset, we analyzed the expression levels of ZNF197-AS1 and its correlation with miR-425 and GABARAPL1, an essential autophagy-related gene. Our analysis revealed that ZNF197-AS1 acts as a ceRNA by competitively binding to miR-425, resulting in the upregulation of GABARAPL1. This interaction plays a crucial role in the growth and metastasis of UM. The expression of GABARAPL1 showed a strong correlation with the clinical outcomes of UM patients. Furthermore, in vitro assays confirmed that ZNF197-AS1 impedes UM cell proliferation, migration, and invasion by modulating the miR-425/GABARAPL1 axis. These findings suggest that ZNF197-AS1 can effectively inhibit UM progression through this ceRNA regulatory network. This study provides valuable insights into the molecular mechanisms underlying UM and highlights the potential of targeting the ZNF197-AS1/miR-425/GABARAPL1 axis as a therapeutic strategy for UM.","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0000,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of physiology. Cell physiology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1152/ajpcell.00457.2024","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

This study investigates the role of the long non-coding RNA (lncRNA) ZNF197-AS1 in uveal melanoma (UM), focusing on its function within a competing endogenous RNA (ceRNA) network. Utilizing the UM-related TCGA dataset, we analyzed the expression levels of ZNF197-AS1 and its correlation with miR-425 and GABARAPL1, an essential autophagy-related gene. Our analysis revealed that ZNF197-AS1 acts as a ceRNA by competitively binding to miR-425, resulting in the upregulation of GABARAPL1. This interaction plays a crucial role in the growth and metastasis of UM. The expression of GABARAPL1 showed a strong correlation with the clinical outcomes of UM patients. Furthermore, in vitro assays confirmed that ZNF197-AS1 impedes UM cell proliferation, migration, and invasion by modulating the miR-425/GABARAPL1 axis. These findings suggest that ZNF197-AS1 can effectively inhibit UM progression through this ceRNA regulatory network. This study provides valuable insights into the molecular mechanisms underlying UM and highlights the potential of targeting the ZNF197-AS1/miR-425/GABARAPL1 axis as a therapeutic strategy for UM.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

ZNF197-AS1/miR-425/GABARAPL1轴：葡萄膜黑色素瘤的新型调控机制

本研究调查了长非编码 RNA（lncRNA）ZNF197-AS1 在葡萄膜黑色素瘤（UM）中的作用，重点研究了它在竞争性内源性 RNA（ceRNA）网络中的功能。利用 UM 相关的 TCGA 数据集，我们分析了 ZNF197-AS1 的表达水平及其与 miR-425 和 GABARAPL1（一种重要的自噬相关基因）的相关性。我们的分析表明，ZNF197-AS1 通过与 miR-425 竞争性结合，起到了 ceRNA 的作用，从而导致 GABARAPL1 的上调。这种相互作用在 UM 的生长和转移中起着至关重要的作用。GABARAPL1 的表达与 UM 患者的临床预后密切相关。此外，体外实验证实 ZNF197-AS1 通过调节 miR-425/GABARAPL1 轴阻碍了 UM 细胞的增殖、迁移和侵袭。这些发现表明，ZNF197-AS1 可通过这一 ceRNA 调控网络有效抑制 UM 的发展。这项研究为研究UM的分子机制提供了有价值的见解，并凸显了靶向ZNF197-AS1/miR-425/GABARAPL1轴作为UM治疗策略的潜力。

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分钟内获得全文去求助

来源期刊

American journal of physiology. Cell physiology 生物-生理学

CiteScore

9.10

自引率

1.80%

发文量

252

审稿时长

1 months

期刊介绍： The American Journal of Physiology-Cell Physiology is dedicated to innovative approaches to the study of cell and molecular physiology. Contributions that use cellular and molecular approaches to shed light on mechanisms of physiological control at higher levels of organization also appear regularly. Manuscripts dealing with the structure and function of cell membranes, contractile systems, cellular organelles, and membrane channels, transporters, and pumps are encouraged. Studies dealing with integrated regulation of cellular function, including mechanisms of signal transduction, development, gene expression, cell-to-cell interactions, and the cell physiology of pathophysiological states, are also eagerly sought. Interdisciplinary studies that apply the approaches of biochemistry, biophysics, molecular biology, morphology, and immunology to the determination of new principles in cell physiology are especially welcome.