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。

Cancer biotherapy & radiopharmaceuticals Pub Date : 2022-11-01 Epub Date: 2021-03-30 DOI:10.1089/cbr.2020.4184
Hua Han, Xiaofeng Xu
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引用次数: 3

摘要

背景:microRNA (miR)-205和GATA结合蛋白3 (GATA3)均与宫颈癌(CC)有关,但其相关性尚不清楚。材料与方法:收集临床宫颈组织标本。采用Kaplan-Meier曲线分析miR-205和GATA3高、低表达CC患者的生存率。分别采用细胞计数试剂盒-8法、划痕法和成管法测定CC细胞活力、迁移和成管。通过TargetScan预测miR-205和GATA3之间的潜在结合位点,并通过双荧光素酶报告基因试验证实。根据需要采用实时荧光定量聚合酶链式反应(qRT-PCR)和Western blot检测miR-205、GATA3、血管内皮生长因子、E-cadherin、N-cadherin、vimentin的相对表达量。结果:CC中MiR-205升高,GATA3降低,两者呈负相关。上调miR-205可提高miR-205的表达和CC细胞活力,促进迁移和小管形成,降低GATA3的表达,而下调miR-205则相反。GATA3是miR-205的靶基因,通过逆转miR-205对迁移和成管相关蛋白表达的影响,逆转了miR-205对CC细胞中GATA3表达和细胞活力、迁移和成管的影响。结论:MiR-205在体外通过靶向GATA3促进CC细胞活力、迁移和成管,为MiR-205在CC中的作用提供了新的证据,也为CC的治疗提供了可能的方法。临床试验注册号:ZLK-20181103-01。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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.

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