{"title":"miR-490-5p inhibits the progression of osteosarcoma by targeting HDAC2.","authors":"Huiqun Jiang, Jiahao Xia, Yuan Tao, Yu Zhang","doi":"10.21037/tcr-2024-2217","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Osteosarcoma (OS) is the most prevalent malignant bone tumor and has a particularly unfavorable prognosis. Although miR-490-5p is regarded as an established diagnostic and predictive marker for human cancers, the role of miR-490-5p in OS remains presently unclear. The aim of this study was to clarify the function of miR-490-5p in OS.</p><p><strong>Methods: </strong>Bioinformatics analysis of OS cells was performed to identify differentially expressed microRNAs (miRNAs, miRs). Then, the expression profiles of miR-490-5p in various OS cells were determined by real-time polymerase chain reaction analysis. The roles of miR-490-5p in OS cells were assessed through <i>in vitro</i> cytological experiments. Bioinformatics methods were used to predict target genes. The relationship between miR-490-5p and HDAC2 was demonstrated by a dual-luciferase reporter gene assay.</p><p><strong>Results: </strong>Expression of miR-490-5p was relatively decreased in OS cells. Overexpression of miR-490-5p inhibited proliferation and metastasis of OS cells. Moreover, miR-490-5p was found to negatively regulate HDAC2 as a downstream target gene. Recovery experiments confirmed that HDAC2 overexpression rescued the inhibitory effect on OS progression by overexpression of miR-490-5p.</p><p><strong>Conclusions: </strong>MiR-490-5p directly regulated HDAC2 expression, thereby modulating the growth and metastatic capacity of OS cells. The miR-490-5p/HDAC2 axis could serve as a promising therapeutic target for OS.</p>","PeriodicalId":23216,"journal":{"name":"Translational cancer research","volume":"14 7","pages":"4357-4368"},"PeriodicalIF":1.7000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12335688/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational cancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21037/tcr-2024-2217","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/7/22 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background: Osteosarcoma (OS) is the most prevalent malignant bone tumor and has a particularly unfavorable prognosis. Although miR-490-5p is regarded as an established diagnostic and predictive marker for human cancers, the role of miR-490-5p in OS remains presently unclear. The aim of this study was to clarify the function of miR-490-5p in OS.
Methods: Bioinformatics analysis of OS cells was performed to identify differentially expressed microRNAs (miRNAs, miRs). Then, the expression profiles of miR-490-5p in various OS cells were determined by real-time polymerase chain reaction analysis. The roles of miR-490-5p in OS cells were assessed through in vitro cytological experiments. Bioinformatics methods were used to predict target genes. The relationship between miR-490-5p and HDAC2 was demonstrated by a dual-luciferase reporter gene assay.
Results: Expression of miR-490-5p was relatively decreased in OS cells. Overexpression of miR-490-5p inhibited proliferation and metastasis of OS cells. Moreover, miR-490-5p was found to negatively regulate HDAC2 as a downstream target gene. Recovery experiments confirmed that HDAC2 overexpression rescued the inhibitory effect on OS progression by overexpression of miR-490-5p.
Conclusions: MiR-490-5p directly regulated HDAC2 expression, thereby modulating the growth and metastatic capacity of OS cells. The miR-490-5p/HDAC2 axis could serve as a promising therapeutic target for OS.
期刊介绍:
Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.