{"title":"LncRNA XIST Promotes Proliferation, Migration and Invasion of Esophageal Squamous Cell Carcinoma Cells <i>via</i> Regulation of miR-186-5p/ZEB1.","authors":"Yunyun Ma, Lili Qian, Dechao Wang, Changyan Chen","doi":"10.21873/anticanres.17477","DOIUrl":null,"url":null,"abstract":"<p><strong>Background/aim: </strong>Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) are crucial molecules for tumor progression in various human cancers. However, the function of lncRNA X-inactive specific transcript (XIST) in esophageal squamous cell carcinoma (ESCC) remains to be determined. The current study aimed to explore the function and molecular mechanism of lncRNA XIST in ESCC progression.</p><p><strong>Materials and methods: </strong>The expression level of lncRNA XIST in ESCC cell lines was measured by qRT-PCR. The effects of lncRNA XIST on cell proliferation, migration, and invasion on ESCC were detected by CCK-8, transwell, and scratch assays. The expression levels of proteins were determined by western blot and luciferase reporter assays were used to identify specific target relationships.</p><p><strong>Results: </strong>LncRNA XIST was overexpressed in ESCC cell lines when compared to normal cell lines. The inhibitor of lncRNA XIST markedly inhibited ESCC cell proliferation, migration, and invasion. Furthermore, miR-186-5p was down-regulated in ESCC cells. LncRNA XIST could sponge miR-186-5p and knockdown of lncRNA XIST could increase the expression of miR-186-5p. We also confirmed Zinc finger E-box binding homeobox 1 (ZEB1) as the target for miR-186-5p, while overexpression of ZEB1 reversed the effects of miR-186-5p inhibition on the malignant behavior of EC9706 and KYSE30 cells.</p><p><strong>Conclusion: </strong>Our data revealed that lncRNA XIST promotes ESCC metastasis by regulating the miR-186-5p/ZEB1 axis. This study may provide a theoretical basis for the molecular mechanisms involved in esophageal cancer.</p>","PeriodicalId":8072,"journal":{"name":"Anticancer research","volume":"45 3","pages":"897-908"},"PeriodicalIF":1.6000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anticancer research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.21873/anticanres.17477","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Background/aim: Accumulating evidence has indicated that long non-coding RNAs (lncRNAs) are crucial molecules for tumor progression in various human cancers. However, the function of lncRNA X-inactive specific transcript (XIST) in esophageal squamous cell carcinoma (ESCC) remains to be determined. The current study aimed to explore the function and molecular mechanism of lncRNA XIST in ESCC progression.
Materials and methods: The expression level of lncRNA XIST in ESCC cell lines was measured by qRT-PCR. The effects of lncRNA XIST on cell proliferation, migration, and invasion on ESCC were detected by CCK-8, transwell, and scratch assays. The expression levels of proteins were determined by western blot and luciferase reporter assays were used to identify specific target relationships.
Results: LncRNA XIST was overexpressed in ESCC cell lines when compared to normal cell lines. The inhibitor of lncRNA XIST markedly inhibited ESCC cell proliferation, migration, and invasion. Furthermore, miR-186-5p was down-regulated in ESCC cells. LncRNA XIST could sponge miR-186-5p and knockdown of lncRNA XIST could increase the expression of miR-186-5p. We also confirmed Zinc finger E-box binding homeobox 1 (ZEB1) as the target for miR-186-5p, while overexpression of ZEB1 reversed the effects of miR-186-5p inhibition on the malignant behavior of EC9706 and KYSE30 cells.
Conclusion: Our data revealed that lncRNA XIST promotes ESCC metastasis by regulating the miR-186-5p/ZEB1 axis. This study may provide a theoretical basis for the molecular mechanisms involved in esophageal cancer.
期刊介绍:
ANTICANCER RESEARCH is an independent international peer-reviewed journal devoted to the rapid publication of high quality original articles and reviews on all aspects of experimental and clinical oncology. Prompt evaluation of all submitted articles in confidence and rapid publication within 1-2 months of acceptance are guaranteed.
ANTICANCER RESEARCH was established in 1981 and is published monthly (bimonthly until the end of 2008). Each annual volume contains twelve issues and index. Each issue may be divided into three parts (A: Reviews, B: Experimental studies, and C: Clinical and Epidemiological studies).
Special issues, presenting the proceedings of meetings or groups of papers on topics of significant progress, will also be included in each volume. There is no limitation to the number of pages per issue.