{"title":"Circ_0084615 promotes epithelial-mesenchymal transition-mediated tumor progression in hepatocellular carcinoma","authors":"Yu Wu, Li Peng","doi":"10.1002/ags3.12828","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Aim</h3>\n \n <p>CircRNAs have been identified as crucial regulators in tumorigenesis and progression. This study aimed to explore the biological role and underlying mechanism of circ_0084615 in hepatocellular carcinoma (HCC).</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>The expression of RNAs was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The effects of circ_0084615 silencing on malignant behaviors of HCC cells were assessed by CCK-8, colony formation, wound healing, and Transwell assays in vitro and tumor transplantation experiment in vivo. The expression of proteins was detected by Western blotting. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation were performed to explore the mechanism of circ_0084615.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>A significant upregulation of circ_0084615 was observed in HCC tissues, and positively correlated with the TNM staging. Silencing of circ_0084615 impeded HCC cell viability, colony formation, migration, invasion, epithelial-mesenchymal transition, and xenograft tumor growth. Mechanistically, circ_0084615 could bind to miR-1200 and eliminate its ability to destroy actin-like 6A (ACTL6A) mRNA, thereby increasing ACTL6A expression and facilitating the malignant behaviors of HCC cells.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p>This study clarified the oncogenic activity and mechanism of circ_0084615, thereby providing potential diagnostic biomarker and therapeutic target for inhibiting HCC progression.</p>\n </section>\n </div>","PeriodicalId":8030,"journal":{"name":"Annals of Gastroenterological Surgery","volume":"8 6","pages":"1107-1117"},"PeriodicalIF":2.9000,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ags3.12828","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annals of Gastroenterological Surgery","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/ags3.12828","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Aim
CircRNAs have been identified as crucial regulators in tumorigenesis and progression. This study aimed to explore the biological role and underlying mechanism of circ_0084615 in hepatocellular carcinoma (HCC).
Methods
The expression of RNAs was detected by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The effects of circ_0084615 silencing on malignant behaviors of HCC cells were assessed by CCK-8, colony formation, wound healing, and Transwell assays in vitro and tumor transplantation experiment in vivo. The expression of proteins was detected by Western blotting. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation were performed to explore the mechanism of circ_0084615.
Results
A significant upregulation of circ_0084615 was observed in HCC tissues, and positively correlated with the TNM staging. Silencing of circ_0084615 impeded HCC cell viability, colony formation, migration, invasion, epithelial-mesenchymal transition, and xenograft tumor growth. Mechanistically, circ_0084615 could bind to miR-1200 and eliminate its ability to destroy actin-like 6A (ACTL6A) mRNA, thereby increasing ACTL6A expression and facilitating the malignant behaviors of HCC cells.
Conclusions
This study clarified the oncogenic activity and mechanism of circ_0084615, thereby providing potential diagnostic biomarker and therapeutic target for inhibiting HCC progression.