微小RNA-612通过下调NOB1抑制卵巢癌细胞的致瘤性。
miRNA-612 suppresses ovarian cancer cell tumorigenicity by downregulating NOB1.
作者信息
Shi Zhikun, Zhou Xu, Bao Meijing, Jia Rongxia, Chu Yuqing, Lin Yang
机构信息
Department of Gynecology and Obstetrics, The Second Hospital of Jilin University Changchun 130041, Jilin, China.
出版信息
Am J Transl Res. 2022 Jun 15;14(6):3904-3914. eCollection 2022.
MicroRNAs (miRNAs) play crucial roles in cancer progression. Our previous study demonstrated that NIN1/RPN12 binding protein 1 homolog (NOB1) was a functional regulator in the progression of ovarian cancer (OC). However, the role of miRNA-612 (miR-612) in OC has not been elucidated. In this study, we aimed to investigate the regulatory mechanism of NOB1 targeting miRNA, miR-612, in OC tumorigenicity. The miR-612 expression was down-regulated in OC patient tissues and four OC cell lines (Caov3, A2780, SKOV3 and OVCAR3). The miR-612 level was negatively correlated with NOB1 expression, and dual-luciferase reporter assay indicated that miR-612 suppressed NOB1 expression by targeting the 3'UTR of NOB1 transcript. Up-regulation of miR-612 mediated by lentiviral transduction suppressed cell proliferation, colony formation, migration, invasion, and induced apoptosis in OC cell lines. In addition, miR-612 overexpression inhibited tumor growth of OC by sequestering NOB1 expression. In conclusion, our results suggested that miR-612 directly targeted NOB1 to suppress OC progression. Therefore, the miR-612-NOB1 axis could serve as therapeutic targets for OC.
微小RNA（miRNA）在癌症进展中发挥着关键作用。我们之前的研究表明，NIN1/RPN12结合蛋白1同源物（NOB1）是卵巢癌（OC）进展中的一种功能调节因子。然而，miRNA-612（miR-612）在OC中的作用尚未阐明。在本研究中，我们旨在探讨NOB1靶向miRNA miR-612在OC致瘤性中的调控机制。miR-612在OC患者组织和四种OC细胞系（Caov3、A2780、SKOV3和OVCAR3）中表达下调。miR-612水平与NOB1表达呈负相关，双荧光素酶报告基因检测表明miR-612通过靶向NOB1转录本的3'UTR抑制NOB1表达。慢病毒转导介导的miR-612上调抑制了OC细胞系的细胞增殖、集落形成、迁移、侵袭，并诱导了细胞凋亡。此外，miR-612过表达通过抑制NOB1表达抑制了OC的肿瘤生长。总之，我们的结果表明miR-612直接靶向NOB1以抑制OC进展。因此，miR-612-NOB1轴可作为OC的治疗靶点。
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