Long non-coding RNA FOXD2-AS1 promotes proliferation, migration and invasion of ovarian cancer cells via regulating the expression of miR-4492

长链非编码RNA FOXD2-AS1通过调控miR-4492的表达促进卵巢癌细胞的增殖、迁移和侵袭。

阅读:1

Abstract

The aim of the present study was to determine the role of long non-coding RNA (lncRNA) forkhead box D2 antisense 1 (FOXD2-AS1) in the development of ovarian cancer, investigate the underlying mechanisms and provide a potential diagnostic biomarker for ovarian cancer. A total of 39 ovarian cancer patients were included, and the ovarian cancer tissues and paracancer tissues were obtained. The ovarian cancer cell lines SKOV3 and OVCAR3 and the human ovarian normal epithelial cell line IOSE80 were cultured. The expression of lncRNA FOXD2-AS1 and miR-4492 was detected by reverse transcription-quantitative PCR. Small interfering RNA targeting FOXD2-AS1 (si-FOXD2-AS1), microRNA (miR)-4492 mimics, miR-4492 inhibitor and their corresponding controls were transfected into cells. The proliferation was detected with a Cell-Couting-Kit-8 assay, and migration and invasion were determined using Transwell assays. The mutual binding site of lncRNA FOXD2-AS1 and miR-4492 was predicted with the miRDB database and verified by a luciferase reporter assay. Finally, a rescue assay was performed. The results suggested that lncRNA FOXD2-AS1 was upregulated in ovarian cancer tissues and cell lines. si-FOXD2-AS1 was able to inhibit the proliferation, migration and invasion of ovarian cancer cells. lncRNA FOXD2-AS1 was confirmed to directly target miR-4492. The expression of lncRNA FOXD2-AS1 and miR-4492 exhibited a negative correlation. In a rescue experiment, miR-4492 inhibitor abrogated the effect of siFOXD2-AS1 in SKOV3 and OVCAR3 cell lines. In conclusion, lncRNA FOXD2-AS1 promotes the proliferation and invasion of ovarian cancer cells via regulating the expression of miR-4492. It may be a novel potential diagnostic biomarker and therapeutic target for ovarian cancer.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。