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miR-532-3p 通过靶向 TROAP 抑制透明细胞肾细胞癌的细胞活力、迁移和侵袭。

MiR-532-3p suppresses cell viability, migration and invasion of clear cell renal cell carcinoma through targeting TROAP.

机构信息

Department of Urology, Tangshan Central Hospital, Tangshan, Hebei, P.R. China.

出版信息

Cell Cycle. 2021 Aug;20(16):1578-1588. doi: 10.1080/15384101.2021.1953767. Epub 2021 Jul 21.

Abstract

Clear cell renal cell carcinoma (ccRCC) is a subtype of renal cell cancer with the highest mortality, infiltration, and metastasis rate, threatening human health. Despite oncogenic role of TROAP in various cancers, its function in ccRCC remains to be unraveled. The differentially expressed mRNAs (DEmRNAs) and miRNAs (DEmiRNAs) were obtained by analyzing the related data sets of ccRCC in TCGA. The expression levels of mRNAs and miRNAs in the cell were detected by qRT-PCR, while the protein levels were characterized by western blot. The viability, migratory and invasive abilities of ccRCC cells were determined by MTT, wound healing and cell invasion assays. The combination of miRNA target site prediction and dual-luciferase reporter gene assay verified the binding relationship between miR-532-3p and TROAP. Research on ccRCC displayed that TROAP expression was upregulated, while miR-532-3p was down-regulated. Besides, upregulation of TROAP could accelerate viability, migratory and invasive potentials of ccRCC cells. On the contrary, miR-532-3p could downregulate TROAP level, but TROAP upregulation reversed the viability, migration, and invasion of ccRCC cells. MiR-532-3p could attenuate the viability, migration and invasion of ccRCC cells by targeting TROAP. This may generate novel insights into molecular therapeutic targets for ccRCC.

摘要

透明细胞肾细胞癌 (ccRCC) 是肾细胞癌的一种亚型,其死亡率、浸润率和转移率最高,威胁着人类健康。尽管 TROAP 在各种癌症中具有致癌作用,但它在 ccRCC 中的功能仍有待揭示。通过分析 TCGA 中 ccRCC 的相关数据集,获得差异表达的 mRNAs (DEmRNAs) 和 miRNAs (DEmiRNAs)。通过 qRT-PCR 检测细胞中 mRNAs 和 miRNAs 的表达水平,通过 Western blot 鉴定蛋白质水平。通过 MTT、划痕愈合和细胞侵袭实验测定 ccRCC 细胞的活力、迁移和侵袭能力。miRNA 靶位预测和双荧光素酶报告基因实验的结合验证了 miR-532-3p 和 TROAP 之间的结合关系。对 ccRCC 的研究表明,TROAP 的表达上调,而 miR-532-3p 下调。此外,TROAP 的上调可加速 ccRCC 细胞的活力、迁移和侵袭潜能。相反,miR-532-3p 可下调 TROAP 水平,但 TROAP 的上调可逆转 ccRCC 细胞的活力、迁移和侵袭。miR-532-3p 通过靶向 TROAP 可减弱 ccRCC 细胞的活力、迁移和侵袭。这可能为 ccRCC 的分子治疗靶点提供新的见解。

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