miRNA-612 suppresses ovarian cancer cell tumorigenicity by downregulating NOB1.

Autor:	Shi Z; Department of Gynecology and Obstetrics, The Second Hospital of Jilin University Changchun 130041, Jilin, China., Zhou X; Department of Gynecology and Obstetrics, The Second Hospital of Jilin University Changchun 130041, Jilin, China., Bao M; Department of Gynecology and Obstetrics, The Second Hospital of Jilin University Changchun 130041, Jilin, China., Jia R; Department of Gynecology and Obstetrics, The Second Hospital of Jilin University Changchun 130041, Jilin, China., Chu Y; Department of Gynecology and Obstetrics, The Second Hospital of Jilin University Changchun 130041, Jilin, China., Lin Y; Department of Gynecology and Obstetrics, The Second Hospital of Jilin University Changchun 130041, Jilin, China.
Jazyk:	angličtina
Zdroj:	American journal of translational research [Am J Transl Res] 2022 Jun 15; Vol. 14 (6), pp. 3904-3914. Date of Electronic Publication: 2022 Jun 15 (Print Publication: 2022).
Abstrakt:	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 in vivo 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. Competing Interests: None. (AJTR Copyright © 2022.)
Databáze:	MEDLINE
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