The objective of this study was to determine the regulatory mechanism of MAGI2-AS3 in clear cell renal cell carcinoma (ccRCC), thereby supplying a new insight for ccRCC treatment. Expression data in TCGA-KIRC were obtained. Target gene lncRNA for research was determined using expression analysis and clinical analysis. lncRNA's downstream regulatory miRNA and mRNA were predicted by bioinformatics databases. ccRCC cell malignant phenotypes were detected via CCK-8, colony formation, Transwell migration, and invasion assays. The targeting relationship between genes was assessed through dual-luciferase reporter gene analysis. Kaplan-Meier (K-M) analysis was carried out to verify the effect of MAGI2-AS3, miR-629-5p, and PRDM16 on the survival rate of ccRCC patients. MAGI2-AS3 expression in ccRCC tissue and cells was shown to be markedly decreased and its expression to continuously decline with tumor progression. MAGI2-AS3 suppresses ccRCC proliferation and migration. Dual-luciferase assay showed that MAGI2-AS3 binds miR-629-5p and that miR-629-5p binds PRDM16. In addition, functional experiments showed that MAGI2-AS3 facilitates PRDM16 expression by repressing miR-629-5p expression, thereby suppressing ccRCC cell aggression. K-M analysis showed that upregulation of either MAGI2-AS3 or PRDM16 significantly improves ccRCC patient survival, while upregulation of miR-629-5p has no significant impact. MAGI2-AS3 sponges miR-629-5p to modulate PRDM16 to mediate ccRCC development. Meanwhile, the MAGI2-AS3/miR-629-5p/PRDM16 axis, as a regulatory pathway of ccRCC progression, may be a possible therapeutic target and prognostic indicator of ccRCC.

中文翻译：

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长非编码 RNA MAGI2-AS3 通过调节 miR-629-5p/PRDM16 轴抑制透明细胞肾细胞癌的细胞进展

本研究的目的是确定MAGI2-AS3在透明细胞肾细胞癌（ccRCC）中的调节机制，从而为ccRCC的治疗提供新的见解。获得了 TCGA-KIRC 中的表达数据。通过表达分析和临床分析确定了研究的靶基因lncRNA。通过生物信息学数据库预测lncRNA的下游调控miRNA和mRNA。通过 CCK-8、集落形成、Transwell 迁移和侵袭实验检测 ccRCC 细胞恶性表型。通过双荧光素酶报告基因分析评估基因之间的靶向关系。进行Kaplan-Meier（KM）分析以验证MAGI2-AS3、miR-629-5p和PRDM16对ccRCC患者生存率的影响。MAGI2-AS3在ccRCC组织和细胞中的表达显着下降，并且其表达随着肿瘤进展而持续下降。MAGI2-AS3 抑制 ccRCC 增殖和迁移。双荧光素酶测定显示 MAGI2-AS3 结合 miR-629-5p，miR-629-5p 结合 PRDM16。此外，功能实验表明，MAGI2-AS3通过抑制miR-629-5p表达来促进PRDM16表达，从而抑制ccRCC细胞的攻击。KM 分析显示，MAGI2-AS3 或 PRDM16 的上调可显着改善 ccRCC 患者的生存率，而 miR-629-5p 的上调则没有显着影响。MAGI2-AS3 海绵 miR-629-5p 调节 PRDM16 介导 ccRCC 发育。同时，MAGI2-AS3/miR-629-5p/PRDM16轴作为ccRCC进展的调节通路，可能是ccRCC的可能治疗靶点和预后指标。