{"title":"MiR-205通过靶向GATA3促进体外宫颈癌细胞的活力、迁移和管状形成。","authors":"Hua Han, Xiaofeng Xu","doi":"10.1089/cbr.2020.4184","DOIUrl":null,"url":null,"abstract":"<p><p><b><i>Background:</i></b> Both microRNA (miR)-205 and GATA Binding Protein 3 (<i>GATA3</i>) were involved in cervical cancer (CC), yet their correlation remained poorly understood. The authors' study aimed to unveil their correlation in CC. <b><i>Materials and Methods:</i></b> Clinical cervical tissue samples were collected. Survival rates of CC patients with high or low miR-205 and <i>GATA3</i> expressions were analyzed using Kaplan-Meier curve. CC cell viability, migration, and tube formation were measured by cell counting kit-8 assay, scratch assay, and tube formation assay, respectively. The potential binding sites between miR-205 and <i>GATA3</i> were predicted by TargetScan, and confirmed with dual-luciferase reporter assay. Relative expressions of miR-205, <i>GATA3</i>, vascular endothelial growth factor, E-cadherin, N-cadherin, and vimentin were quantified with quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. <b><i>Results:</i></b> MiR-205 was increased, yet <i>GATA3</i> was decreased in CC, indicating that they were negatively correlated. Upregulating miR-205 increased miR-205 expression and CC cell viability and promoted migration and tube formation, yet decreased <i>GATA3</i> expression, while downregulating miR-205 exerted the opposite effects. <i>GATA3</i> was the target gene of miR-205, and reversed the effect of miR-205 on <i>GATA3</i> expression and cell viability, migration, and tube formation in CC cells by reversing the effects of miR-205 on migration- and tube formation-related protein expressions. <b><i>Conclusion:</i></b> MiR-205 promotes CC cell viability, migration, and tube formation <i>in vitro</i> by targeting <i>GATA3</i>, providing new evidence for the implication of miR-205 in CC and a possible therapeutic method for CC. Clinical Trial Registration number: ZLK-20181103-01.</p>","PeriodicalId":518937,"journal":{"name":"Cancer biotherapy & radiopharmaceuticals","volume":" ","pages":"779-791"},"PeriodicalIF":0.0000,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"3","resultStr":"{\"title\":\"MiR-205 Promotes the Viability, Migration, and Tube Formation of Cervical Cancer Cells <i>In Vitro</i> by Targeting <i>GATA3</i>.\",\"authors\":\"Hua Han, Xiaofeng Xu\",\"doi\":\"10.1089/cbr.2020.4184\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b><i>Background:</i></b> Both microRNA (miR)-205 and GATA Binding Protein 3 (<i>GATA3</i>) were involved in cervical cancer (CC), yet their correlation remained poorly understood. The authors' study aimed to unveil their correlation in CC. <b><i>Materials and Methods:</i></b> Clinical cervical tissue samples were collected. Survival rates of CC patients with high or low miR-205 and <i>GATA3</i> expressions were analyzed using Kaplan-Meier curve. CC cell viability, migration, and tube formation were measured by cell counting kit-8 assay, scratch assay, and tube formation assay, respectively. The potential binding sites between miR-205 and <i>GATA3</i> were predicted by TargetScan, and confirmed with dual-luciferase reporter assay. Relative expressions of miR-205, <i>GATA3</i>, vascular endothelial growth factor, E-cadherin, N-cadherin, and vimentin were quantified with quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. <b><i>Results:</i></b> MiR-205 was increased, yet <i>GATA3</i> was decreased in CC, indicating that they were negatively correlated. Upregulating miR-205 increased miR-205 expression and CC cell viability and promoted migration and tube formation, yet decreased <i>GATA3</i> expression, while downregulating miR-205 exerted the opposite effects. <i>GATA3</i> was the target gene of miR-205, and reversed the effect of miR-205 on <i>GATA3</i> expression and cell viability, migration, and tube formation in CC cells by reversing the effects of miR-205 on migration- and tube formation-related protein expressions. <b><i>Conclusion:</i></b> MiR-205 promotes CC cell viability, migration, and tube formation <i>in vitro</i> by targeting <i>GATA3</i>, providing new evidence for the implication of miR-205 in CC and a possible therapeutic method for CC. Clinical Trial Registration number: ZLK-20181103-01.</p>\",\"PeriodicalId\":518937,\"journal\":{\"name\":\"Cancer biotherapy & radiopharmaceuticals\",\"volume\":\" \",\"pages\":\"779-791\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer biotherapy & radiopharmaceuticals\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1089/cbr.2020.4184\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2021/3/30 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer biotherapy & radiopharmaceuticals","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1089/cbr.2020.4184","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2021/3/30 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
MiR-205 Promotes the Viability, Migration, and Tube Formation of Cervical Cancer Cells In Vitro by Targeting GATA3.
Background: Both microRNA (miR)-205 and GATA Binding Protein 3 (GATA3) were involved in cervical cancer (CC), yet their correlation remained poorly understood. The authors' study aimed to unveil their correlation in CC. Materials and Methods: Clinical cervical tissue samples were collected. Survival rates of CC patients with high or low miR-205 and GATA3 expressions were analyzed using Kaplan-Meier curve. CC cell viability, migration, and tube formation were measured by cell counting kit-8 assay, scratch assay, and tube formation assay, respectively. The potential binding sites between miR-205 and GATA3 were predicted by TargetScan, and confirmed with dual-luciferase reporter assay. Relative expressions of miR-205, GATA3, vascular endothelial growth factor, E-cadherin, N-cadherin, and vimentin were quantified with quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. Results: MiR-205 was increased, yet GATA3 was decreased in CC, indicating that they were negatively correlated. Upregulating miR-205 increased miR-205 expression and CC cell viability and promoted migration and tube formation, yet decreased GATA3 expression, while downregulating miR-205 exerted the opposite effects. GATA3 was the target gene of miR-205, and reversed the effect of miR-205 on GATA3 expression and cell viability, migration, and tube formation in CC cells by reversing the effects of miR-205 on migration- and tube formation-related protein expressions. Conclusion: MiR-205 promotes CC cell viability, migration, and tube formation in vitro by targeting GATA3, providing new evidence for the implication of miR-205 in CC and a possible therapeutic method for CC. Clinical Trial Registration number: ZLK-20181103-01.