Background: Epithelial ovarian cancer (EOC) stands up for about 90% of ovarian cancer cases, which is the frequent cause of death among women. LncRNAs are involved in progression of EOC. Meanwhile, lncRNA SNHG17 was upregulated in EOC, while the detailed function of SNHG17 in EOC remains unclear.
Methods: Protein and mRNA levels were assessed by western blot and RT-qPCR, respectively. The function of SNHG17 in EOC cells was tested by CCK-8, Ki-67 staining, flow cytometry and transwell assay. Dual luciferase was applied for assessing the relation among SNHG17, miR-485-5p and AKT1. Furthermore, in vivo experiments were applied to test the impact of SNHG17 in EOC.
Results: SNHG17 knockdown reduced the proliferation and promoted the apoptosis of EOC cells. Consistently, si-SNHG17 obviously reduced the invasion and epithelial-to-mesenchymal transition (EMT) process of EOC cells. MiR-485-5p was proved to be the target miRNA of SNHG17, and SNHG17 negatively regulated the level of miR-485-5p. MiR-485-5p inhibitor significantly abolished the anti-tumor impact of si-SNHG17 on EOC. AKT1 was identified to be targeted by miR-485-5p, and miR-485-5p negatively modulated AKT1 and p-mTOR levels. Moreover, miR-485-5p mimics reduced the proliferation, migration and promoted the apoptosis of EOC cells via targeting AKT1. Furthermore, si-SNHG17 markedly suppressed EOC growth in vivo.
Conclusion: SNHG17 silencing inhibits the development of EOC via regulation of miR-485-5p/AKT1 axis. Thus, our study might supply a novel strategy against EOC.
Keywords: AKT1; Epithelial ovarian cancer; SNHG17; mTOR; miR-485-5p.
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