Department of Gynaecology and Obstetrics, Jinshan Hospital affiliated to Fudan University, Shanghai 201508, China.
Department of Gynaecology and Obstetrics, Jinshan Hospital affiliated to Fudan University, Shanghai 201508, China.
Biomed Pharmacother. 2019 Feb;110:850-856. doi: 10.1016/j.biopha.2018.11.104. Epub 2018 Dec 14.
MicroRNA-542-3p (miR-542-3p) has been implicated in several cancers; however, its precise role in ovarian cancer is unclear. In this study, we found that miR-542-3p was significantly downregulated in epithelial ovarian cancer (EOC) tissues and cell lines. Functional assays showed that overexpression of miR-542-3p suppressed tumor cell proliferation, migration, and invasion in vitro, whereas miR-542-3p knockdown dramatically promoted tumor cell proliferation and invasion. An in vivo assay also revealed that miR-542-3p overexpression significantly attenuated tumor growth. Mechanistically, the gene of cyclin-dependent kinase 14 (CDK14) was identified as a novel target of miR-542-3p. CDK14 overexpression reversed the suppressive effects of miR-542-3p in ovarian cancer cells. Collectively, these results suggest that miR-542-3p functions as a tumor-suppressive miRNA in ovarian cancer by directly targeting CDK14. Our data provide novel insights into potential future treatments for patients with ovarian cancer.
微小 RNA-542-3p(miR-542-3p)在多种癌症中都有涉及;然而,其在卵巢癌中的确切作用尚不清楚。在这项研究中,我们发现 miR-542-3p 在卵巢上皮性癌(EOC)组织和细胞系中明显下调。功能分析表明,miR-542-3p 的过表达可抑制体外肿瘤细胞的增殖、迁移和侵袭,而 miR-542-3p 的敲低则显著促进肿瘤细胞的增殖和侵袭。体内实验也表明 miR-542-3p 的过表达可显著抑制肿瘤生长。机制上,细胞周期蛋白依赖性激酶 14(CDK14)基因被鉴定为 miR-542-3p 的一个新的靶基因。CDK14 的过表达逆转了 miR-542-3p 对卵巢癌细胞的抑制作用。综上所述,这些结果表明 miR-542-3p 通过直接靶向 CDK14 在卵巢癌中发挥肿瘤抑制 miRNA 的作用。我们的数据为卵巢癌患者的潜在未来治疗提供了新的见解。