{"title":"miR-30d-5p represses the proliferation, migration, and invasion of lung squamous cell carcinoma via targeting <i>DBF4</i>.","authors":"Yitian Qi, Yi Hou, Liangchen Qi","doi":"10.1080/26896583.2021.1926855","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>This study aims to explore the mechanism of miR-30d-5p in regulating the development of lung squamous cell carcinoma (LUSC) via targeting <i>DBF4</i>.</p><p><strong>Methods: </strong>Bioinformatics methods were employed to analyze the differentially expressed genes in LUSC tissue microarray. qRT-PCR was employed to detect the expression of miR-30d-5p and <i>DBF4</i> mRNA in normal human bronchial epithelial cells and LUSC cells. CCK-8 was used to detect LUSC cell activity. Wound healing assay was employed to detect the migratory ability of LUSC cells. Transwell was employed to detect invasive ability. Dual-luciferase reporter assay was used to detect the targeting relationship between miR-30d-5p and <i>DBF4</i>. Western blot was used to detect the protein expression of marker molecules associated with epithelial-mesenchymal transition (EMT).</p><p><strong>Results: </strong>In this study, the expression of miR-30d-5p in LUSC cell lines was found to be obviously low compared with that in normal human bronchial epithelial cell line, which was opposite to the expression of <i>DBF4</i>. Dual-luciferase reporter assay verified that miR-30d-5p could target <i>DBF4</i> and the overexpression of miR-30d-5p downregulated the expression of <i>DBF4</i>. Overexpression of <i>DBF4</i> promoted the proliferation, migration, invasion, and EMT of LUSC, whereas over-expression of miR-30d-5p could weaken the promotion of <i>DBF4</i> on cancer cells.</p><p><strong>Conclusion: </strong>miR-30d-5p downregulates the expression of <i>DBF4</i> to regulate the development of LUSC.</p>","PeriodicalId":53200,"journal":{"name":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","volume":"39 3","pages":"251-268"},"PeriodicalIF":1.2000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"8","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis","FirstCategoryId":"93","ListUrlMain":"https://doi.org/10.1080/26896583.2021.1926855","RegionNum":4,"RegionCategory":"环境科学与生态学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/6/24 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"ENVIRONMENTAL SCIENCES","Score":null,"Total":0}
引用次数: 8
Abstract
Objective: This study aims to explore the mechanism of miR-30d-5p in regulating the development of lung squamous cell carcinoma (LUSC) via targeting DBF4.
Methods: Bioinformatics methods were employed to analyze the differentially expressed genes in LUSC tissue microarray. qRT-PCR was employed to detect the expression of miR-30d-5p and DBF4 mRNA in normal human bronchial epithelial cells and LUSC cells. CCK-8 was used to detect LUSC cell activity. Wound healing assay was employed to detect the migratory ability of LUSC cells. Transwell was employed to detect invasive ability. Dual-luciferase reporter assay was used to detect the targeting relationship between miR-30d-5p and DBF4. Western blot was used to detect the protein expression of marker molecules associated with epithelial-mesenchymal transition (EMT).
Results: In this study, the expression of miR-30d-5p in LUSC cell lines was found to be obviously low compared with that in normal human bronchial epithelial cell line, which was opposite to the expression of DBF4. Dual-luciferase reporter assay verified that miR-30d-5p could target DBF4 and the overexpression of miR-30d-5p downregulated the expression of DBF4. Overexpression of DBF4 promoted the proliferation, migration, invasion, and EMT of LUSC, whereas over-expression of miR-30d-5p could weaken the promotion of DBF4 on cancer cells.
Conclusion: miR-30d-5p downregulates the expression of DBF4 to regulate the development of LUSC.