Zhang Jingyu, Lu Qingbo, Pang Haigang, Zhang Min, Wei Wenhai
Department of Urology, The Fourth People's Hospital of Shenyang Shenyang 110031, Liaoning Province, China.
Department of Emergency, Ningyang County First People's Hospital Tai'an 271400, Shandong Province, China.
Am J Transl Res. 2021 Nov 15;13(11):12694-12703. eCollection 2021.
We investigated the mechanism of miR-103a-3p-mediated renal cell carcinoma (RCC) progression.
The miR-103a-3p expressions were measured in clinical samples and in two RCC cell lines. MiR-103a-3p was inhibited or over-expressed in the 786-O and UO31 cell lines, respectively.
We found that miR-103a-3p is closely related to the development of RCC cells. A bioinformatics analysis and a dual-luciferase reporter gene assay revealed that there is a direct interaction between TMEM33 and miR-103a-3p. Moreover, a rescue assay further confirmed that TMEM33 overexpression can attenuate miR-103a-3p-induced RCC cell development.
miR-103a-3p exerts a carcinogenic function in RCC by regulating TMEM33, a finding that may provide new insights into the development of prognostic markers and therapeutic targets for RCC.
我们研究了miR-103a-3p介导肾细胞癌（RCC）进展的机制。
检测临床样本及两种肾癌细胞系中miR-103a-3p的表达。分别在786-O和UO31细胞系中抑制或过表达miR-103a-3p。
我们发现miR-103a-3p与肾癌细胞的发展密切相关。生物信息学分析和双荧光素酶报告基因检测显示，跨膜蛋白33（TMEM33）与miR-103a-3p之间存在直接相互作用。此外，一项挽救实验进一步证实，TMEM33过表达可减弱miR-103a-3p诱导的肾癌细胞发展。
miR-103a-3p通过调节TMEM33在肾细胞癌中发挥致癌作用，这一发现可能为肾细胞癌预后标志物和治疗靶点的开发提供新见解。
