Effects of CDKN2B-AS1 on cellular proliferation, invasion and AKT3 expression are attenuated by miR-424-5p in a model of ovarian endometriosis

Sixue Wang, Wang S, Mingyu Yi, Yi M, Xinyue Zhang, Zhang X, Tingting Zhang, Zhang T, Li Jiang, Jiang L, Cao L, Le Cao, Yuxin Zhou, Zhou Y, Xiaoling Fang, Fang X
Reproductive BioMedicine Online · 2021 · vol. 42(6) , pp. 1057–1066 · doi:10.1016/j.rbmo.2021.02.004 · PMID:33820740 · W3132517252
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The lncRNA CDKN2B-AS1 promotes ovarian endometriosis cell proliferation and invasion, but its effects are suppressed by miR-424-5p, which also downregulates AKT3 expression.

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Abstract

RESEARCH QUESTION: Endometriosis is a common and complicated gynaecologic disease. Long non-coding RNA CDKN2B-AS1 plays a crucial role in the development and progression of several cancers. Whether CDKN2B-AS1 contributes to endometriosis, however, remains unknown. DESIGN: Cellular proliferation, invasion and DNA synthesis abilities were assessed by CCK8, transwell and 5-ethynyle-2'-deoxyuridine assays. The expression of epithelial-mesenchymal transition markers and three isoforms of AKT was detected using Western blot. Real-time polymerase chain reaction was used to determine the relative expression levels of CDKN2B-AS1 and candidate miRNAs in ectopic, eutopic endometria and normal endometrial tissues. The relationship between CDKN2B-AS1 and miRNA was determined by luciferase reporter assays. RESULTS: The relative expression level of CDKN2B-AS1 was up-regulated in eutopic and ectopic endometria. In endometrial stromal cells and Ishikawa cells, CDKN2B-AS1 overexpression promoted cellular proliferation and invasion, and increased the protein expression of vimentin but decreased the expression of E-cadherin. miR-424-5p was confirmed the target of CDKN2B-AS1 through bioinformatics tools and luciferase reporter assays. In addition, the enhanced effect of cellular phenotype of CDKN2B-AS1 overexpression was significantly attenuated by miR-424-5p overexpression. Furthermore, miR-424-5p was able to directly target AKT3 through luciferase reporter assay. Mechanistically, CDKN2B-AS1 acts as a ceRNA by sponging miR-424-5p and targets AKT3. CONCLUSIONS: The cellular mechanism of CDKN2B-AS1 in endometriosis was confirmed; CDKN2B-AS1 may be a potential target for ovarian endometriosis therapy.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis MicroRNAs Ovarian Diseases Proto-Oncogene Proteins c-akt RNA, Long Noncoding Adult Adult Endometriosis Endometriosis Endometriosis Epithelial-Mesenchymal Transition Epithelial-Mesenchymal Transition Female Female Humans Humans MicroRNAs MicroRNAs Middle Aged Middle Aged

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