{"title":"Dysregulation of miR-204-5p/APLN axis affects malignant progression and cell stemness of esophageal cancer","authors":"Yifan Zhou, Ruihong Xu, Jinlong Luo, Xiangwei Li, Yonglong Zhong, Zhendong Sun","doi":"10.1016/j.mrfmmm.2022.111791","DOIUrl":null,"url":null,"abstract":"<div><h3>Objective</h3><p>This study attempted to investigate the mechanism of miR-204-5p and its downstream gene in regulating bio-functions of esophageal cancer (EC).</p></div><div><h3>Methods</h3><p>Bioinformatics analysis was performed to select the mature miRNAs<span><span>, mRNAs, and clinical data of EC. The miRNA-mRNA regulatory axis was predicted through bioinformatics and used Dual-luciferase analysis to verify the interaction between miR-204-5p and APLN. qRT-PCR was applied to analyze expression of miR-204-5p and APLN mRNA. Western blot was utilized to detect APLN </span>protein expression. Functional assays like CCK-8, wound healing, Transwell, and stem cell sphere formation assays were launched to confirm proliferative, migratory, invasive and stemness of cells in different treatment groups.</span></p></div><div><h3>Results</h3><p>MiR-204-5p was lowly expressed while its target gene APLN was highly expressed in tumor tissues. Besides, miR-204-5p overexpression hindered proliferation, invasion, migration, and stemness of EC cells. Additionally, dual-luciferase assay verified the interaction of miR-204-5p and APLN. MiR-204-5p could downregulate APLN level and its overexpression reduced the effect of APLN on EC cell functions.</p></div><div><h3>Conclusion</h3><p>Dysregulation of miR-204-5p/APLN axis was linked with malignant progression of EC. MiR-204-5p/APLN may be an underlying candidate for the design of anticarcinogens.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"825 ","pages":"Article 111791"},"PeriodicalIF":1.5000,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0027510722000185","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
引用次数: 1
Abstract
Objective
This study attempted to investigate the mechanism of miR-204-5p and its downstream gene in regulating bio-functions of esophageal cancer (EC).
Methods
Bioinformatics analysis was performed to select the mature miRNAs, mRNAs, and clinical data of EC. The miRNA-mRNA regulatory axis was predicted through bioinformatics and used Dual-luciferase analysis to verify the interaction between miR-204-5p and APLN. qRT-PCR was applied to analyze expression of miR-204-5p and APLN mRNA. Western blot was utilized to detect APLN protein expression. Functional assays like CCK-8, wound healing, Transwell, and stem cell sphere formation assays were launched to confirm proliferative, migratory, invasive and stemness of cells in different treatment groups.
Results
MiR-204-5p was lowly expressed while its target gene APLN was highly expressed in tumor tissues. Besides, miR-204-5p overexpression hindered proliferation, invasion, migration, and stemness of EC cells. Additionally, dual-luciferase assay verified the interaction of miR-204-5p and APLN. MiR-204-5p could downregulate APLN level and its overexpression reduced the effect of APLN on EC cell functions.
Conclusion
Dysregulation of miR-204-5p/APLN axis was linked with malignant progression of EC. MiR-204-5p/APLN may be an underlying candidate for the design of anticarcinogens.
期刊介绍：
Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs.
MR publishes articles in the following areas:
Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence.
The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance.
Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing.
Landscape of somatic mutations and epimutations in cancer and aging.
Role of de novo mutations in human disease and aging; mutations in population genomics.
Interactions between mutations and epimutations.
The role of epimutations in chromatin structure and function.
Mitochondrial DNA mutations and their consequences in terms of human disease and aging.
Novel ways to generate mutations and epimutations in cell lines and animal models.
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