| Journal of Ovarian Research | |
| Long non-coding RNA AFAP1-AS1 facilitates ovarian cancer progression by regulating the miR-107/PDK4 axis | |
| Xiaoyu Yang1  Yuhan Sun1  Bao Liu1  Yugang Chi1  Li Yan1  | |
| [1] Chongqing Health Center for Women and Children, 401147, Chongqing, China; | |
| 关键词: AFAP1-AS1; Ovarian cancer (OC); MiR-107; PDK4; | |
| DOI : 10.1186/s13048-021-00808-x | |
| 来源: Springer | |
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【 摘 要 】
BackgroundAbnormally expressed in various tumors, long non-coding RNAs (lncRNAs) feature prominently in tumor development, yet little is still known regarding the functional roles of lncRNA AFAP1 antisense RNA 1 (AFAP1-AS1) in ovarian cancer (OC).MethodsThe relative expression levels of lncRNA AFAP1-AS1, microRNA (miR)-107 and pyruvate dehydrogenase kinase isozyme 4 (PDK4) mRNA were assessed by quantitative real-time PCR. PDK4, PCNA and cyclin D1 expression levels were determined using Western blot analysis. Bioinformatics analysis and dual-luciferase gene reporter assay were conducted for identifying and validating the binding sequences between AFAP1-AS1 and miR-107, as well as between miR-107 and PDK4. Cell counting kit-8 assay was employed for detecting cell proliferation. Cell migration and invasion abilities were examined using Transwell assays.ResultsThe present study revealed that AFAP1-AS1 expression was elevated in OC cells and tissues. AFAP1-AS1 expression and FIGO stage were positively correlated. AFAP1-AS1 knockdown repressed OC cell proliferation, migration and invasion. AFAP1-AS1 functioned as a sponge of miR-107, and miR-107 reversed the effects of AFAP1-AS1 on OC cells. It was validated that miR-107 was able to bind to PDK4, and AFAP1-AS1 regulated PDK4 expression by competitively binding with miR-107. Additionally, miR-107 modulated OC cell proliferation, migration and invasion via targeting PDK4.ConclusionsLncRNA AFAP1-AS1 serves as a tumor driver in the pathogenesis of OC via the miR-107/PDK4 axis.
【 授权许可】
CC BY
【 预 览 】
| Files | Size | Format | View |
|---|---|---|---|
| RO202107032331655ZK.pdf | 3988KB |
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